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Abstract Background It is necessary to determine whether there are adverse health effects of prenatal exposure to long-term, low levels of mercury and selenium. However, there are limited that reports on the association between mercury levels by selenium levels and birth size. Therefore, we examined whether maternal mercury levels during pregnancy had any effect on infant birth size, and size, and whether selenium levels influenced this relationship. Objectives To examine the association between mercury and selenium levels during pregnancy with infant birth size. Methods The Japan Environment and Children's Study is a prospective birth cohort conducted between 2011 and 2014. Total mercury levels and total selenium levels in maternal blood during the second and third trimesters were measured using Inductively Coupled Plasma-Mass Spectrometry. Birth weight and small-for-gestational-age were confirmed by medical records. Small-for-gestational-age was defined as birth weight below the 10th percentile according to standard percentile for gender, parity, and gestational age. Multiple linear and logistic regression analyses were used to examine the association between maternal mercury exposure and birth weight or small-for-gestational-age adjusted for confounders (including maternal age and body mass index pregnancy). Results Overall, 15,444 pregnant women were included in this study. Median (inter-quartile range) of blood mercury and selenium levels were 3.66 (2.59–5.18) ng/g and 170.0 (158.0–183.0) ng/g, respectively. Compared to infants of mothers with the highest blood selenium level, those of mothers with the lowest blood selenium level had neither a significant birth weight increase (9 g, 95% confidence interval: −6, 25) nor a significant odds ratio for small-for-gestational-age (0.903, 95% confidence interval: 0.748, 1.089). Compared to infants of mothers with the lowest blood mercury level, those of mothers with the highest blood mercury level had neither a significant birth weight reduction (−12 g, 95% confidence interval: −27, 4) nor a significant odds ratio for small-for-gestational-age (0.951, 95% confidence interval: 0.786, 1.150). Compared to infants of mothers with the lowest quartile of maternal blood mercury level, all infants of mothers with the highest quartile of maternal blood mercury level had a reduced birth head circumference of 0.073 cm (95% confidence interval: −0.134, −0.011). Conclusions There was no association between maternal blood mercury levels and small-for-gestational-age and birth weight among 15,444 pregnant women. In a Japanese population, which has a relatively higher blood mercury level than reported in Western population, reduced birth size was not found to be associated with blood mercury levels, with the exception of birth head circumference. Highlights • We examined association between maternal mercury and selenium with birth outcomes. • 15,444 pregnant Japanese women were included in the prospective birth cohort study. • An association between blood mercury and birth head circumference was found. • No association between blood selenium and birth size was found. • Increased small-for-gestational-age from blood mercury levels was not observed. [ABSTRACT FROM AUTHOR]

Abstract Objective Selenium seems to be a risk factor for diabetes mellitus (DM) in recent studies, opposite to the previous expectation that it may contribute to prevent DM. The authors aimed to ascertain the relationship between selenium and DM. Methods Data were collected from the National Health and Nutrition Examination Survey conducted from 2011 to 2014. A multivariate logistic regression analysis with adjustment for age, sex, race/ethnicity, hypertension, dyslipidemia and body mass index was conducted to evaluate the odds ratio for DM. Results The total number of subjects was 19,931. Large proportion of subjects were excluded due to young age (< 20 years) and missing data. The data of 3406 participants were analyzed, and a total of 604 had DM. In a multivariate logistic regression model, the increase of 10 μg/L in selenium increased the prevalence of DM by 12% (OR: 1.12; 95% CI: 1.06–1.18). Further analysis with 1:1 propensity score matching data with age and sex showed a similar results (OR: 1.08; 95% CI: 1.01–1.15). In addition, the restricted cubic spline regression showed a dose-dependent relationship between selenium level and DM. Subgroup analysis showed a dose-dependent relationship between selenium level and DM regardless of sex or race/ethnicity Conclusions This large population study clearly demonstrates a positive association between selenium level and DM. This finding could have implications for nutritional supplementation in clinical settings. [ABSTRACT FROM AUTHOR]

Background Selenoprotein synthesis requires the reinterpretation of a UGA stop codon as one that encodes selenocysteine (Sec), a process that requires a set of dedicated translation factors. Among the mammalian selenoproteins, Selenoprotein P (SELENOP) is unique as it contains a selenocysteine-rich domain that requires multiple Sec incorporation events. Scope of review In this review we elaborate on new data and current models that provide insight into how SELENOP is made. Major conclusions SELENOP synthesis requires a specific set of factors and conditions. General significance As the key protein required for proper selenium distribution, SELENOP stands out as a lynchpin selenoprotein that is essential for male fertility, proper neurologic function and selenium metabolism. [ABSTRACT FROM AUTHOR]

Background: Selenium, an essential trace element, has been investigated as a potential cancer prevention agent. However, several studies have indicated that selenium supplementation may be associated with an increased risk of type 2 diabetes (T2D), although an equivocal relation of this nature requires confirmation.Objective: We examined the association between baseline plasma concentrations of selenium and the prevalence of T2D, as well as whether participant characteristics or intake of other antioxidant nutrients modified this relation.Methods: We conducted cross-sectional analyses of 1727 participants from the Selenium Trial, a randomized clinical trial of selenium supplementation for colorectal adenoma chemoprevention that had data for baseline selenium plasma concentrations, T2D status, and dietary intake. Logistic regression modeling was used to evaluate the associations between plasma selenium concentrations and prevalent T2D, adjusting for confounding factors. Heterogeneity of effect by participant characteristics was evaluated utilizing likelihood-ratio tests.Results: Mean ± SD plasma selenium concentrations for those with T2D compared with those without T2D were 143.6 ± 28.9 and 138.7 ± 27.2 ng/mL, respectively. After adjustment for confounding, higher plasma selenium concentrations were associated with a higher prevalence of T2D, with ORs (95% CIs) of 1.25 (0.80, 1.95) and 1.77 (1.16, 2.71) for the second and third tertiles of plasma selenium, respectively, compared with the lowest tertile (P-trend = 0.007). No significant effect modification was observed for age, sex, body mass index, smoking, or ethnicity. Increased odds of T2D were seen among those who were in the highest tertile of plasma selenium and the highest category of intake of β-cryptoxanthin (P-trend = 0.03) and lycopene (P-trend = 0.008); however, interaction terms were not significant.Conclusions: These findings show that higher plasma concentrations of selenium were significantly associated with prevalent T2D among participants in a selenium supplementation trial. Future work is needed to elucidate whether there are individual characteristics, such as blood concentrations of other antioxidants, which may influence this relation. [ABSTRACT FROM AUTHOR]

A growing body of evidence indicates that exposure to selenium (Se) can cause neurotoxicity, and this can occur because of its interference with several neurotransmitter systems in humans and animals. Dopamine is a critical modulator of a variety of brain functions and a prime target for environmental neurotoxicants. However, effects of environmentally relevant concentrations of Se on dopaminergic system and its neurobehavioral effects are still largely unknown. For this purpose, we exposed zebrafish, a model organism, to different concentrations of dietary l -selenomethionine (control, 3.5, 11.1, 27.4, and 63.4 μg Se/g dry weight) for a period of 60 days. Cognitive performance of fish was evaluated using a plus maze associative learning paradigm. Oxidative stress, as the main driver of Se neurotoxicity, was assessed by measuring the ratio of reduced to oxidized glutathione (GSH:GSSG), lipid peroxidation (LPO) levels, and mRNA expression of several antioxidant enzymes in the zebrafish brain. Dopamine levels in the brain and the expression of genes involved in dopamine synthesis, storage, reuptake, metabolism, and receptor activation were examined. Moreover, transcription of several synaptic plasticity-related immediate-early and late response genes was determined. Overall, fish fed with the two highest concentrations of dietary Se displayed impaired associative learning. Se exposure also induced oxidative stress in the zebrafish brain, as indicated by a reduction in GSH:GSSG ratio, increased LPO levels, and up-regulation of antioxidant genes in fish treated with the two highest concentrations of Se. An increase in brain dopamine levels associated with altered expression of dopaminergic cell markers was evident in different treatment groups. Moreover, Se exposure led to the down-regulation of immediate-early and late response genes in fish that exhibiting learning impairment. Taken together, the results of this study imply that the induction of oxidative stress and dysregulation of dopaminergic neurotransmission may underlie Se-induced impairment of associative learning in zebrafish. [ABSTRACT FROM AUTHOR]

Inuit in Canada have high selenium intake from the consumption of country food such as fish and marine mammals. The health consequence is not known. This study examines the association between blood selenium concentration and prevalence of stroke among Canadian Inuit. The International Polar Year Inuit Health Survey was conducted in 2007–2008. Among the 2077 adults participants (≥18 years old) who completed a questionnaire and gave blood samples, 49 stroke cases were reported, 31 of which were from women. The crude prevalence of stroke was 2.4% in the participants. Participants with stroke had lower blood selenium (geometric mean: 260 μg/L vs. 319 μg/L) and dietary selenium (144 μg/day vs. 190 μg/day) compared to individuals without stroke. Participants with high blood/dietary selenium exposure (quartiles 3 and 4) had a lower prevalence of stroke compared to those with low selenium exposure (quartile 1). The adjusted odds ratio ranged from 0.09 to 0.25 among subgroups (e.g. age, sex, and blood mercury). An L-shaped relationship between prevalence of stroke with blood and dietary selenium was observed, based on the cubic restricted spline and segmented regression analyses. The estimated turning points of the L-shaped curve for blood selenium and dietary selenium were 450 μg/L and 350 μg/day, respectively. Below the turning points, it was estimated that each 50-μg/L increase in blood selenium was associated with a 38% reduction in the prevalence of stroke, and each 50-μg/day increase in dietary selenium was associated with a 30% reduction in the prevalence of stroke. In conclusion, blood and dietary selenium are reversely associated with the prevalence of stroke in Inuit, which follows an L-shaped relationship. Whether this relationship applies to other population needs further investigation. [ABSTRACT FROM AUTHOR]

Due the long-term nature of joint tissue remodeling processes, knee structures including meniscus and anterior cruciate ligament (ACL) can be a model for studying the bioaccumulation of mercury (Hg) and selenium (Se). The accumulation and retention of Hg in human tissues can have a negative effect on the proper functioning of homeostasis-affecting organisms. A factor of chronic poisoning with Hg forms is probably the Se:Hg ratio in tissues. Se:Hg molar ratios below one may increase Hg toxicity potentials, while molar ratios that approach or exceed one effectively may protect against Hg toxicity. Therefore, the aim of the study was to determine total mercury (THg), Se, and Se:THg molar ratios in the cartilage, meniscus and ACL of patients with osteoarthritis (OA) from northwestern Poland. In all studied samples (n = 95), we observed higher Se than THg concentration. Taking into consideration the biological factors, we found significantly higher THg levels in the cartilage of women, patients under 65 years of age, patients without hypertension and in the ACL of patients with spinal degenerative disease. We found higher Se levels in the meniscus in women than in men. In all studied parts of the knee joint, we found the Se:THg molar ratio higher than one, which suggests that the joint forming structures are not much exposed to THg. Moreover the results reported here may provide a basis for establishing reference values for the meniscus and ACL in patients with OA who had undergone knee replacement surgery. [ABSTRACT FROM AUTHOR]

Project Varicocele is an abnormal tortuosity and distension of the veins of the pampiniform plexus in the spermatic cord. It is the most common surgically correctable cause of male infertility. Several studies have revealed the effects of increased oxidative stress on serum, semen, and testicular tissues in patients with varicocele or in animal models. The aim of this study was to investigate the effects of sodium selenite on testicular damage induced by experimental left varicocele in male Wistar rats. Procedure In the present study, the effects of oral administration of sodium selenite (at doses of 0.05, 0.1, 0.2, and 0.4 mg/kg bw) were assessed in normal and varicocelized rats. Results The varicocelized control rats showed decrease in sperm quality parameters, decreased activity of testes CAT, GPX and SOD, increased levels of MDA, and damage in testicular architecture. Administration of sodium selenite significantly reduced these changes to nearly normal levels, but did not change these parameters in normal rats. Histopathological studies further confirmed the protective effects of sodium selenite on varicocele-induced testicular damage in rats. Administrations of sodium selenite did not change these parameters in normal rats. Conclusions Taken together, the results of this study suggest that sodium selenite treatment may have beneficial effect on the testes of varicocelized rats. [ABSTRACT FROM AUTHOR]

To explore the metabolism of T-2 toxin in human chondrocytes (HCs) and determine the impact of selenium supplementation. For determination of cytotoxicity using the MTT assay, optical density values were read with an automatic enzyme-linked immunosorbent assay reader at 510 nm. Cell survival was calculated and the cytotoxicity estimated. To identify the metabolites of T-2 toxin, the medium supernatants and C28/I2 cells were analyzed by high-performance liquid chromatography tandem mass spectrometry (HPLC–MS/MS) separately. For HPLC–MS/MS, the mobile phase A was water and phase B was 98% methanol. The gradient for the elution was: 0–0.5 min, 50% of B; 0.5–2.0 min, 100% of B; 2.0–3.5 min, 100% of B; 3.6–6 min, 50% of B. T-2 toxin increased the toxicity to C28/I2 cells significantly in a dose- and time-dependent manner (viability range 91.5–22.0%). Supplementation with selenium (100 ng/mL) could increase the cell viability after the 24 h incubation. The concentration of T-2 toxin in the cell medium decreased from 20 to 6.67 ± 1.02 ng/mL, and the concentration of HT-2 toxin increased from 0 to 6.88 ± 1.23 ng/mL during the 48 h incubation, whereas the relative concentration of T-2 toxin in cells increased from 0 to 12.80 ± 1.84 ng/g. Supplementary selenium in the HCs cultures reduced the cytotoxicity induced by T-2 toxin significantly, and was associated with rapid conversion of T-2 toxin in the culture medium to HT-2 toxin. T-2 toxin was more toxic to HCs than HT-2 toxin at equivalent concentrations. HT-2 toxin was a detectable metabolite of T-2 toxin in cultured HCs, and selenium enhanced the metabolic conversion of T-2 toxin, reducing its cytotoxicity to HCs. [ABSTRACT FROM AUTHOR]

This study investigated whether plasma selenium levels modified the risk for prostate cancer (PC) related to arsenic exposure. We conducted a case-control study that included 318 PC patients and 318 age-matched, healthy control subjects. Urinary arsenic profiles were examined using HPLC-HG-AAS and plasma selenium levels were measured by ICP-MS. We found that plasma selenium levels displayed a significant dose-dependent inverse association with PC. The odds ratio (OR) and 95% confidence interval (CI) for PC was 0.07 (0.04–0.13) among participants with a plasma selenium level >28.06 μg/dL vs. ≤19.13 μg/dL. A multivariate analysis showed that participants with a urinary total arsenic concentration >29.28 μg/L had a significantly higher OR (1.75, 1.06–2.89) for PC than participants with ≤29.89 μg/L. The combined presence of a low plasma selenium level and a high urinary total arsenic concentration exponentially increased the OR for PC, and additively interacted with PSA at levels ≥20 ng/mL. This is the first epidemiological study to examine the combined effects of plasma selenium and urinary total arsenic levels on the OR for PC. Our data suggest a low plasma selenium level coupled with a high urinary total arsenic concentration creates a significant risk for aggressive PC. [ABSTRACT FROM AUTHOR]

Introduction Several studies have shown an inverse relationship between selenium status and cardiovascular health, although epidemiologic evidence yielded by the randomized trials did not find a beneficial effect of selenium administration. The aim of this study was to analyze the association between serum selenium levels and lipid profile adjusted by age, sex and other associated factors among a general adult population in Spain. Materials and methods We recruited 372 hospital employee volunteers (60 men and 312 women) with a mean age of 47 (SD: 10.9), whom were given a standardized questionnaire. Serum selenium concentration was measured by electrothermal atomization atomic absorption spectrometry. Serum copper and zinc concentrations were measured using flame atomic absorption spectrometry. Results The mean of serum selenium was 79.5 μg/L (SD: 11.7) with no sex-dependent differences. In the multivariate linear regression analysis, the associated factors with the mean levels of selenium were: age (β = 0.223; CI 95%: 0.101–0.345), p < 0.001; widowhood (β = −9.668; CI 95%: −17.234 to −2.102), p = 0.012; calcium supplements (β = 3.949; CI 95%: 0.059–7.838), p = 0.047; zinc (β = 0.126; CI 95%: 0.013–0.238), p = 0.028 and glucose (β = 0.172; CI 95%: 0.062- 0.281), p = 0.002; Participants with serum selenium ≥ 79.5 μg/L were 1.98 (OR = 1.98; CI 95% 1.17–3.35; p = 0.011) and 2.04 times (OR = 2.04; CI 95% 1.06–3.97; p = 0.034) more likely to have cholesterol ≥200 mg/dL and LDL-c ≥100 mg/dL respectively than those with serum selenium <79.5 μg/L. Conclusions Higher selenium was positively associated with increased total and LDL cholesterol but not with HDL-c and triglycerides. More studies are needed in order to confirm the lower serum selenium findings in widows. [ABSTRACT FROM AUTHOR]

Selenium is involved in the complex system of defense against oxidative stress in diabetes through its biological function of selenoproteins and the antioxidant enzyme. A case-control study was carried out to determine the association of plasma selenium with oxidative stress and body composition status presented in Type 2 Diabetes Mellitus (T2DM) patient and healthy control. This study involved 82 newly diagnosed T2DM patients and 82 healthy controls. Plasma selenium status was determined with Graphite Furnace Atomic Absorption Spectrometry. Body Mass Index, total body fat and visceral fat was assessed for body composition using Body Composition Analyzer (TANITA). Oxidative DNA damage and total antioxidant capacity were determined for oxidative stress biomarker status. In age, gender and BMI adjustment, no significant difference of plasma selenium level between T2DM and healthy controls was observed. There was as a significant difference of Oxidative DNA damage and total antioxidant capacity between T2DM patients and healthy controls with tail DNA% 20.62 [95% CI: 19.71,21.49] (T2DM), 17.67 [95% CI: 16.87,18.56] (control); log tail moment 0.41[95% CI: 0.30,0.52] (T2DM), 0.41[95% CI: 0.30,0.52] (control); total antioxidant capacity 0.56 [95% CI: 0.54,0.58] (T2DM), 0.60 [95% CI: 0.57,0.62] (control). Waist circumference, BMI, visceral fat, body fat and oxidative DNA damage in the T2DM group were significantly lower in the first plasma selenium tertile (38.65–80.90 μg/L) compared to the second (80.91–98.20 μg/L) and the third selenium tertiles (98.21–158.20 μg/L). A similar trend, but not statistically significant, was observed in the control group. [ABSTRACT FROM AUTHOR]

Objective Wide variation exists in ovarian cancer incidence rates suggesting the importance of environmental factors. Due to increasing environmental pollution, trace elements and heavy metals have drawn attention in studies defining the etiology of cancer, but scant data is available for ovarian cancer. Our aim was to compare the tissue concentrations of lead, selenium and nickel in epithelial ovarian cancer, borderline tumor and healthy ovarian tissues. Methods The levels of lead, selenium and nickel were estimated using atomic absorption spectrophotometry in formalin-fixed paraffin-embedded tissue samples. Tests were carried out in 20 malignant epithelial ovarian cancer, 15 epithelial borderline tumor and 20 non-neoplastic healthy ovaries. Two samples were collected for borderline tumors, one from papillary projection and one from the smooth surface of cyst wall. Results Pb and Ni concentrations were found to be higher both in malignant and borderline tissues than those in healthy ovaries. Concentrations of Pb and Ni in malignant tissues, borderline papillary projections and capsular tissue samples were not different. Comparison of Se concentrations of malignant, borderline and healthy ovarian tissues did not reveal statistical difference. Studied metal levels were not found to be different in either papillary projection or in cyst wall of the borderline tumors. Conclusions This study revealed the accumulation of lead and nickel in ovarian tissue is associated with borderline and malignant proliferation of the surface epithelium. Accumulation of these metals in epithelial ovarian cancer and borderline ovarian tumor has not been demonstrated before. [ABSTRACT FROM AUTHOR]

Selenium supplementation of the diets of rodents has consistently been shown to suppress mammary carcinogenesis and some, albeit not all, human epidemiological studies have indicated an inverse association between selenium and breast cancer risk. In order to better understand the role selenium plays in breast cancer, 30 samples of tumor tissue were obtained from women with breast cancer and analyzed for selenium concentration, the levels of several selenium-containing proteins and the levels of the MnSOD anti-oxidant protein. Polymorphisms within the genes for these same proteins were determined from DNA isolated from the tissue samples. There was a wide range of selenium in these tissues, ranging from 24 to 854 ng/gm. The selenium levels in the tissues were correlated to the genotype of the SELENOP selenium carrier protein, but not to other proteins whose levels have been reported to be responsive to selenium availability, including GPX1, SELENOF and SBP1. There was an association between a polymorphism in the gene for MnSOD and the levels of the encoded protein. These studies were the first to examine the relationship between selenium levels, genotypes and protein levels in human tissues. Furthermore, the obtained data provide evidence for the need to obtain data about the effects of selenium in breast cancer by examining samples from that particular tissue type. [ABSTRACT FROM AUTHOR]

Mercury (Hg) is likely bound to large biomolecules (e.g. proteins) in living organisms, and in order to assess Hg metabolic pathways and possible toxicological effects, it is essential to study these Hg containing biomolecules. However, the exact nature of most metal binding biomolecules is unknown. Such studies are still in their infancy and information on this topic is scarce because the analysis is challenging, mainly due to their lability upon digestion or extraction from the tissue. New analytical methods that allow complex Hg-biomolecules to be analysed intact are needed and only few very recent studies deal with this approach. Therefore, as an initial step towards the characterization of Hg containing biomolecules, an analytical procedure has been optimised using size-exclusion chromatography (SEC) with inductively coupled plasma mass spectrometry (ICP-MS) detection. We applied this technique to elucidate the distribution and elution profile of Hg and Se, and some physiological important elements such as Fe, Ni, Zn and Cu, to assess metal binding profiles in liver and kidney samples of red deer ( Cervus elaphus ) and wild boar ( Sus scrofa ) who roam freely within the largest Hg mining district on Earth, Almadén in Spain. Elemental fractionation profiles of the extracts from different tissues were obtained using two different SEC columns (BioSep-SEC-S2000 GL 300–1 kDa and Superdex 75 10/300 GL 70–3 kDa). Similar profiles of Hg were observed in red deer and wild boar; however, significant differences were evident for liver and kidney. Moreover, the profiles of Se showed a single peak at high-medium molecular weight in all investigated tissues, while co-elution of Hg with Fe, Ni, Zn and Cu was observed. [ABSTRACT FROM AUTHOR]

Aims Selenium (Se) and zinc (Zn) are trace elements required for optimal brain functions. Thus, the role of Se and Zn against protein malnutrition induced oxidative stress on mitochondrial antioxidants and electron transport chain (ETC) enzymes from rats' brain were investigated. Main methods Normal protein (NP) and low protein (LP) rats were fed with diets containing 16% and 5% casein respectively for a period of 10 weeks. Then the rats were supplemented with Se and Zn at a concentration of 0.15 mg L − 1 and 227 mg L − 1 in drinking water for 3 weeks after which the rats were sacrificed. Key findings The results obtained from the study showed significant (p < 0.05) increase in lipid peroxidation (LPO), ROS production, oxidized glutathione (GSSG) levels and mitochondrial swelling and significant (p < 0.05) reductions in catalase (CAT) and Mn-superoxide dismutase (Mn-SOD) activities, glutathione (GSH) levels, GSH/GSSG ratio and MTT reduction as a result of LP ingestion. The activities of mitochondrial ETC enzymes were also significantly inhibited in both the cortex and cerebellum of LP-fed rats. Supplementation with either Se or Zn restored the alterations in all the parameters. Significance The study showed that Se and Zn might be beneficial in protecting mitochondrial antioxidants and ETC enzymes against protein malnutrition induced oxidative stress. [ABSTRACT FROM AUTHOR]

In this study, we investigated the protective effect of selenium (Se) on cisplatin (Cis) induced testicular damage using histopathological, immunohistochemical and biochemical approaches. Twenty-one male Wistar rats were equally divided into three groups of seven rats each: control (C), Cis, and Cis + Se. Cis and Cis + Se group rats received Cis at a dose of 12 mg/kg b.w./day, intraperitoneally for 3 consecutive days. Cis + Se group rats received selenium via oral gavage 3 mg/kg/day (twice-a day as 1.5 mg/kg) until 11th consecutive days starting at 5 days before cisplatin injection. C group received only 0.9% NaCl intraperitoneally and orally at same time and at equal volume. After the treatment, the histopathological, immunohistochemical and biochemical examinations were performed. In seminiferous tubules of Cis treated rats were observed the most consistent findings characterized with vacuolization, desquamation, disorganization, and also was a considerable reduction in elongated spermatids, however the Cis + Se group exhibited improved histopathologic changes. In the immunohistochemical examinations, caspase-3 immunopositive cells displayed higher in the Cis group according to C and Cis + Se groups. Bcl-2 and NF-κB staining revealed a moderate number in the C group and significantly fewer in the Cis group compared to the Cis + Se groups. Additionally, MDA levels were also significantly increased in the Cis group in comparison to Control group, but pretreatment with selenium prevented elevation of MDA levels significantly in Cis + Se group rats. This study indicates that Cis-treatment induced testicular apoptosis and lipid peroxidation, and combined treatment with selenium prevented severity of the toxicity in rats. [ABSTRACT FROM AUTHOR]

We conducted a detailed assessment of the maternal transfer of mercury and selenium to eggs in three bird species ( n = 107 parents and n = 339 eggs), and developed predictive equations linking contaminant concentrations in eggs to those in six tissues of the mother (blood, muscle, liver, kidney, breast feathers, and head feathers). Mercury concentrations in eggs were positively correlated with mercury concentrations in each of the mother's internal tissues ( R 2 ≥ 0.95), but generally not with feathers. For each species, the proportion of mercury transferred to eggs decreased as mercury concentrations in the mother increased. At the same maternal mercury concentration, the proportion of mercury transferred to eggs differed among species, such that Forster's tern ( Sterna forsteri ) and black-necked stilt ( Himantopus mexicanus ) females transferred more methylmercury to their eggs than American avocet ( Recurvirostra americana ) females. Selenium concentrations in eggs also were correlated with selenium concentrations in the mother's liver ( R 2 = 0.87). Furthermore, mercury and selenium concentrations in tern eggs were positively correlated with those in the father ( R 2 = 0.84). Incubating male terns had 21% higher mercury concentrations in blood compared to incubating females at the same egg mercury concentration. We provide equations to predict contaminant concentrations in eggs from each of the commonly sampled bird tissues. [ABSTRACT FROM AUTHOR]

Selenium (Se) is shown to be an essential element for sow nutrition and a great deal of information has been accumulated for the last two decades indicating that dietary form of Se is a major determinant of its efficiency. Indeed, there are two major Se sources for pigs, namely inorganic selenium (mainly selenite or selenate) and organic selenium in the form of selenomethionine (SeMet; mainly as Se-yeast or SeMet preparations). The aim of the review is to update existing information about Se roles in sow nutrition with a specific emphasis to the oxidative stress and possibilities of decreasing negative consequences of the stresses by using dietary Se supplementation in an optimal form. It has been clearly shown that organic selenium has many important advantages in sow nutrition in comparison to traditional sodium selenite. The aforementioned benefits of organic selenium for sow include: better Se status of sows, especially in the case of advanced parities; improved antioxidant defences of sows; increased Se concentration in colostrum and milk and improved antioxidant status of colostrum and milk; improved Se transfer via placenta; improved Se status of foetus and development of pig embryos. It was proven that replacement of sodium selenite by organic Se in the sow's diet improved Se status of newly born piglets characterised by increased Se concentrations in tissues and whole body. In particular, increased Se concentration in piglet muscles could be considered as an important storage form of Se to be used in stress conditions. Furthermore, organic Se in sow's diet (versus sodium selenite) provides better Se status and antioxidant status of weaning piglets, as well as improves thyroid metabolism and increases activities of major digestive enzymes in piglet pancreas at time of weaning. However, most of the commercially relevant parameters (growth rate, mortality, FCR, etc.) were not affected. Only in two most recent publications in which sodium selenite was replaced by pure organic Se source in the sows diet, there were significant improvements in weaning litter weight and average weight of progeny piglets and daily weight gain of piglet from birth to weaning. Indeed, additional well-designed organic Se trials with big numbers of sows in commercial conditions are needed to explore a full potential of organic Se in sow nutrition. [ABSTRACT FROM AUTHOR]

Lactating mother and her two month old healthy daughter (APGAR 10) gave their scalp hair for a multielement profile analysis; 25 elements were analyzed with the ICP MS. Mother’s hair was divided into 5 cm long segment proximal to the scull ( Young ), and the distal segment further up to the hair tip ( Old ). One centimeter of hair records one month of the metabolic activity of the bioelements in the body. Mother’s Young hair and daughters hair have 2.70 and 9.74 μg g −1 Se, a distinctly higher Se concentrations than the Old hair of 0.87 μg g −1 . The adequate hair Se concentrations in Croatia women population vary from 0.08 to 0.63 μg g −1 ; values below or above that range indicate deficiency or excess, respectively. Dietary recall revealed that during the last trimester of pregnancy and over a period of a week, the mother has consumed 135 g of Brazil nuts ( Bertholletia excelsa ) (BN); BN is an exceptionally rich Se dietary source. The amount of Se in BN varies and one week consumption of 135 g of BN may result in Se daily intake of 367 to 492 μg g −1 day −1 over a period of seven consecutive days, and what is about or exceeds the Upper Limit of daily selenium intake of 400 μg −1 g −1 . The excessively high infant hair Se mirrored a natural high mother to fetus transplacental transfer of bio elements in the last trimester of pregnancy. The potential toxicological risks of such a high Se transfer remains to be elucidated. [ABSTRACT FROM AUTHOR]

Objectives Preeclampsia is a hypertensive disorder of pregnancy which is one of the leading causes of maternal and perinatal mortality and pre-term delivery, especially in low and middle income countries. Selenium is an important constituent of selenoproteins that act as antioxidant and have several metabolic functions. The present study was conducted to determine serum selenium concentration in preeclampsia patients in order to find out the role of selenium in preeclampsia. Methods This study was conducted as case-control study with 74 preeclampsia patients as cases whose gestation were ≥20 weeks (52 mild and 22 severe patients) and 118 normotensive pregnant women as controls from same gestational period. Detailed patient history was recorded during routine hospital visits. Serum selenium concentration was determined by using atomic absorption spectroscopy. Independent sample t -test and Pearson’s correlation test were done for the statistical analysis using the statistical software package SPSS, version 16. Results Our study found that mean serum concentration of selenium in preeclampsia patients was significantly lower than that of healthy pregnant women ( p < 0.05). Further analysis for selenium concentration with disease severity explored that selenium concentration was significantly lower in severe preeclampsia in comparison to mild preeclampsia ( p < 0.05). We found no significant difference for selenium concentration between rural and urban preeclampsia patients ( p > 0.05). Pearson’s correlation analysis reveals significant negative correlation of selenium with systolic blood pressure ( r = −0.419, p = 0.001), diastolic blood pressure ( r = −0.392, p = 0.001), and gestational period ( r = −0.218, p = 0.001). Conclusion Our study found that preeclampsia patients have decreased serum selenium concentration than the healthy pregnant women. [ABSTRACT FROM AUTHOR]

This study was performed to characterise selenium (Se) and Se species in cerebrospinal fluid (CSF) of sheep and its relation to the respective Se concentrations in serum. Paired samples from 10 adult sheep were used for the study. Five sheep were fed a diet with a marginal Se concentration of <0.05 mg Se/kg diet dry weight (dw, Se – ), and five animals were fed the same diet supplemented with sodium selenite revealing a concentration of 0.2 mg Se/kg diet dw (Se + ). The feeding strategy was conducted for two years; The results on metabolic effects were published previously. At the end of the feeding period, paired samples of serum and CSF were collected and analysed using ion exchange chromatography inductively coupled plasma–dynamic reaction cell–mass spectrometry (IEC-ICP-DRC-MS) technique for total Se concentration and concentrations of Se species. Albumin concentrations were analysed additionally. The feeding strategy caused significant differences ( p < 0.01) in serum Se concentrations with 33.1 ± 5.11 μg Se/l in the Se – group and 96.5 ± 18.3 μg Se/l in the Se + group, respectively. The corresponding total Se concentrations in CSF were 4.38 ± 1.02 μg Se/l and 6.13 ± 1.64 μg Se/l in the Se – and the Se + group, respectively, missing statistical significance ( p = 0.077). IEC-ICP-DRC-MS technique was able to differentiate the Se species selenoprotein P-bound Se (SePP), selenomethionine, glutathione peroxidase-bound Se (Se-GPx), selenocystine, thioredoxin reductase-bound Se, ovine serum albumin-bound Se (Se-OSA), SeIV and SeVI in ovine serum and CSF. Quantitatively, SePP is the main selenoprotein in ovine serum followed by Se-GPx. The CSF/blood ratio of albumin (Q Albumin ) reflected a physiological function of the blood-CSF barrier in all sheep. Q Se-species were higher than Q Albumin both feeding groups, supporting the hypothesis of local production of Se species in the brain. Significant positive regression lines for CSF vs. serum were found for albumin and Se-OSA only, suggesting a role of albumin to convey Se across the blood-CSF barrier. The ovine model, together with the IEC-ICP-DRC-MS technique to characterise the Se species, might be a worthwhile model for further studies as repeated sample collection as well as modification of the nutritional status is feasible and effective. [ABSTRACT FROM AUTHOR]

Background Selenium is important for human health and involved in various metabolic processes. Deficiency of selenium associates with increased risk for cancer and cardiovascular diseases. There has been an increase use of selenium supplements for the treatment of autoimmune thyroid conditions. However, the potential biological effects of selenium overload arouse the public concern. The aim of this study was to investigate the associations of plasma selenium concentrations of adults with metabolic syndrome (MS) in Chinese population. Methods A matched case-control study including 204 metabolic syndrome patients and 204 healthy controls was conducted in 2012. The MS cases were defined according to the criteria of Chinese Diabetes Society (CDS). Healthy controls without abnormality of metabolic components were matched with cases in age, gender and region. Plasma concentrations of selenium were determined by graphite furnace atomic absorption spectrometry (GFAAS). Fasting plasma glucose (FPG), total cholesterol (TC), triglycerides (TG), high density lipoprotein cholesterol (HDL), and low density lipoprotein cholesterol (LDL) were detected by automatic biochemical analyzer. Results The median levels of plasma selenium in MS group were 146.3 (107.3–199.4) μg/L, which were significantly higher than that in the control group (127.4: 95.7–176.0) μg/L; Plasma levels of selenium were related to the risk of MS in dose-response manner. Risk of MS was significantly higher in subjects with plasma selenium in the highest tertile (T3: ≥176.0 μg/L) compared to those in the lowest tertile (T1: <95.7 μg/L) [odds ratio (OR) = 2.416 (95% CI: 1.289–4.526)]. The plasma levels of selenium were positively correlated with fasting plasma glucose (FPG) ( r s = 0.268, P < 0.001). Plasma selenium at the median (T2: 95.7–176.0 μg/L) or upper tertile (T3: ≥176.0 μg/L) was associated with increased risk of elevated FPG (defined by FPG ≥ 6.1 mmol/L) as compared with the lowest tertile (T1: ≤95.7 μg/L) [T2 vs. T1, OR = 3.487 (1.738–6.996); T3 vs. T1, OR = 6.245 (3.005–12.981)]. Conclusions Higher levels of plasma selenium might increase the risk of metabolic syndrome and elevated fasting plasma glucose. Selenium supplements should be used with prudence for CVD and cancer prevention. [ABSTRACT FROM AUTHOR]

Observational studies addressing the relation between selenium and human health, particularly cancer risk, yielded inconsistent results, while most recent randomized trials showed a fairly consistent pattern suggesting null or adverse effects of the metalloid. One of the most plausible explanations for such inconsistencies is inadequate exposure assessment in observational studies, commonly carried out by measuring total Se content without taking into account the specific exposure to the individual chemical forms of the metalloid, whose toxic and nutritional properties may vary greatly. Data on the distribution of these species in human blood and their correlation with overall selenium levels are very limited. The concentrations of organic and inorganic selenium species were analyzed in serum of fifty subjects sampled from the general population of the municipality of Modena, northern Italy, aged from 35 to 70 years. Samples were collected during a 30-month period, and determinations of selenium species were carried out using high pressure liquid chromatography coupled with inductively coupled plasma dynamic reaction cell mass spectrometry. The majority of selenium was found to be present as organic species, but the inorganic forms showed higher levels than expected. These species showed limited correlations with age, sex and body mass index, while the organic forms increased in subjects consuming selenium-containing dietary supplements and decreased in smokers. The length of the sample storage period strongly influenced the distribution of selenium compounds, with a clear tendency towards higher inorganic and lower organic selenium levels over time. In multivariate analysis adjusting for potential confounders, total serum selenium correlated with human serum albumin-bound selenium and, in males, with two organic species of the metalloid (selenocysteine and glutathione peroxidase-bound selenium), while little association existed with the other organic forms and the inorganic ones. These findings highlight the potential for exposure misclassification of observational epidemiologic investigations based on overall selenium content in blood and possibly other tissues, and the critical role of the storage conditions for speciation analysis. [ABSTRACT FROM AUTHOR]

A short review is given of the potential role of selenium deficiency and selenium intervention trials in atherosclerotic heart disease. Selenium is an essential constituent of several proteins, including the glutathione peroxidases and selenoprotein P. The selenium intake in Europe is generally in the lower margin of recommendations from authorities. Segments of populations in Europe may thus have a deficient intake that may be presented by a deficient anti-oxidative capacity in various illnesses, in particular atherosclerotic disease, and this may influence the prognosis of the disease. Ischemic heart disease and heart failure are two conditions where increased oxidative stress has been convincingly demonstrated. Some of the intervention studies of anti-oxidative substances that have focused on selenium are discussed in this review. The interrelationship between selenium and coenzyme Q10, another anti-oxidant, is presented, pointing to a theoretical advantage in using both substances in an intervention if there are deficiencies within the population. Clinical results from an intervention study using both selenium and coenzyme Q10 in an elderly population are discussed, where reduction in cardiovascular mortality, a better cardiac function according to echocardiography, and finally a lower concentration of the biomarker NT-proBNP as a sign of lower myocardial wall tension could be seen in those on active treatment, compared to placebo. [ABSTRACT FROM AUTHOR]

Objective Low levels of selenium (Se) and glutathione peroxidase (GSHPx), a key selenoenzyme, were documented in systemic inflammatory response syndrome (SIRS) and sepsis, both associated with high mortality. Se supplementation had mixed effects on outcome. We hypothesized that Se supplementation could have a different impact on biomarkers and 28-day mortality in patients with SIRS vs. sepsis. Methods Adult patients with SIRS or sepsis were randomized to either high-dose (Se+, n = 75) or standard-dose (Se−, n = 75) Se supplementation. Plasma Se, whole blood GSHPx activity, C-reactive protein (CRP), procalcitonin (PCT), prealbumin, albumin and cholesterol levels were measured serially up to day 14. Results There was no difference in mortality between Se− (24/75) vs. Se+ group (19/75; p = 0.367) or between SIRS and septic patients (8/26 vs. 35/124; p = 0.794). There was a trend to reduced mortality in SIRS patients in the Se+ vs. Se− group ( p = 0.084). Plasma Se levels increased in the Se+ group only in patients with sepsis but not in patients with SIRS. Plasma Se levels correlated with GSHPx. In SIRS/Se+ group, Se correlated only with GSHPx. In SIRS/Se− group, Se correlated with cholesterol but not with other biomarkers. In sepsis patients, Se levels correlated with cholesterol, GSHPx and prealbumin. Cholesterol levels were higher in survivors in the Se− group. Conclusions Se levels correlated with GSHPx activity and other nutritional biomarkers with significant differences between SIRS and sepsis groups. High-dose Se supplementation did not affect mortality but a strong trend to decreased mortality in SIRS patients warrants further studies in this population. [ABSTRACT FROM AUTHOR]

Nutritional muscular dystrophy (NMD) of chicks is induced by dietary selenium (Se)/vitamin E (Vit. E) deficiencies and may be associated with oxidative cell damage. To reveal the underlying mechanisms related to the presumed oxidative cell damage, we fed four groups of 1-day-old broiler chicks ( n = 40/group) with a basal diet (BD; 10 μg Se/kg; no Vit. E added, −Se −Vit. E) or the BD plus all-rac-α-tocopheryl acetate at 50 mg/kg (−Se +Vit. E), Se (as sodium selenite) at 0.3 mg/kg (+Se −Vit. E), or both of these nutrients (+Se +Vit. E) for 6 weeks. High incidences of NMD (93%) and mortality (36%) of the chicks were induced by the BD, starting at week 3. Dietary Se deficiency alone also induced muscle fiber rupture and coagulation necrosis in the pectoral muscle of chicks at week 3 and thereafter, with increased ( P < 0.05) malondialdehyde, decreased ( P < 0.05) total antioxidant capacity, and diminished ( P < 0.05) glutathione peroxidase activities in the muscle. To link these oxidative damages of the muscle cells to the Se-deficiency-induced NMD, we first determined gene expression of the potential 26 selenoproteins in the muscle of the chicks at week 2 before the onset of symptoms. Compared with the +Se chicks, the −Se chicks had lower ( P < 0.05) muscle mRNA levels of Gpx1, Gpx3, Gpx4, Sepp1, Selo, Selk, Selu, Selh, Selm, Sepw1, and Sep15 . The −Se chicks also had decreased ( P < 0.05) production of 6 selenoproteins (long-form selenoprotein P (SelP-L), GPx1, GPx4, Sep15, SelW, and SelN), but increased levels ( P < 0.05) of the short-form selenoprotein P in muscle at weeks 2 and 4. Dietary Se deficiency elevated ( P < 0.05) muscle p53, cleaved caspase 3, cleaved caspase 9, cyclooxygenase 2 (COX2), focal adhesion kinase (FAK), phosphatidylinositol 3-kinase (PI3K), phospho-Akt, nuclear factor-κB (NF-κB), p38 mitogen-activated protein kinase (p38 MAPK), phospho-p38 MAPK, phospho-JNK, and phospho-ERK and decreased ( P < 0.05) muscle procaspase 3, procaspase 9, and NF-κB inhibitor α. In conclusion, the downregulation of SelP-L, GPx1, GPx4, Sep15, SelW, and SelN by dietary Se deficiency might account for induced oxidative stress and the subsequent peroxidative damage of chick muscle cells via the activation of the p53/caspase 9/caspase 3, COX2/FAK/PI3K/Akt/NF-κB, and p38 MAPK/JNK/ERK signaling pathways. Metabolism of peroxides and redox regulation are likely to be the mechanisms whereby these selenoproteins prevented the onset of NMD in chicks. [ABSTRACT FROM AUTHOR]

Data from National Health and Nutrition Examination Survey for the period 2011–2012 were used to determine normal reference ranges and percentile distributions for manganese (Mn) and selenium (Se) in blood by gender, age, race/ethnicity, socioeconomic status as determined by annual family income, and smoking status. The effect of gender, age, race/ethnicity, family income, and smoking status on the levels of Mn and Se was also determined by fitting regression models. Males had lower adjusted levels of Mn and higher adjusted levels of Se than females. Adjusted levels of Mn decreased with increase in age but adjusted levels of Se were lower in adolescents aged 12–19 years than adults aged 20–64 years. Non-Hispanic black (NHB) had the lowest levels of both Mn and Se and non-Hispanic Asians (NHAS) had the highest levels of both Mn and Se. Non-Hispanic white (NHW) and NHB had lower levels of Mn than Hispanics (HISP) and NHAS. NHB and HISP had lower levels of Se than NHW and NHAS. Low annual income (<$20,000) was associated with lower levels of Se than high annual income (≥$55,000). Smoking negatively affected the adjusted levels of Se among seniors aged ≥65 years but this was not observed in other age groups. Mn levels were not affected by smoking. [ABSTRACT FROM AUTHOR]

The study aimed at defining the relationship between blood selenium concentration (Se-B) and levels of oxidative stress and antioxidative capacity in healthy children. The studies were conducted on 337 children (mean age: 8.53 ± 1.92 years). The groups of individuals with Se-B <1st quartile (group I, Se-B < 70 μg/L), with Se-B fitting the range of 1st quartile and median (group II, Se-B: 70–76.9 μg/L), with Se-B between the median and 3rd quartile (group III, Se-B: 77–83.9 μg/L) and those with Se-B above the 3rd quartile (group IV, Se-B ≥ 84 μg/L) were distinguished. Level of oxidative stress was defined using determination of urine malonyldialdehyde concentration (MDA) and urine 8-hydroxy-2-deoxyguanosine concentration (8-OHdg). Urine total antioxidant status (TAS) was determined. In group IV TAS was significantly higher than in groups I–III. A positive correlation was detected between Se-B and TAS. In healthy children an appropriately high Se-B seems to ensure higher total antioxidative status. [ABSTRACT FROM AUTHOR]

Selenium metabolic patterns in the human body originating from five distinct selenium dietary sources, selenate, selenite, selenomethionine (SeMet), methylselenocysteine (MeSeCys) and selenized yeast, were investigated by performing concurrent HPLC–mass spectrometric analysis of human serum and urine. Total selenium and selenium species time profiles were generated by sampling and analyzing serum and urine from volunteers treated with selenium supplements, up to 5 and 24 h following ingestion, respectively. We found that an increase in total serum selenium levels, accompanied by elevated selenium urinary excretion, was the common pattern for all treatments, except for that of selenite supplementation. Selenosugar 1 was a universal serum metabolite in all treatments, indicating that ingested selenium is favorably metabolized to the sugar. Except for selenite and selenized yeast ingestion, these patterns were reflected in the urine time series of the different treatments. Selenosugar 1 was the major selenium species present in urine in all treatments except for the selenate treatment, accounting for about 80% of the identified excreted species within 24 h of ingestion. Furthermore, the urinary metabolite trimethylselenonium ion (TMSe) was detected for the first time in human background serum by using HPLC coupled to elemental and molecular mass spectrometry. The concurrent monitoring of non-protein selenium species in both body fluids provides the relation between bioavailability and excretion of the individual ingested species and of their metabolic products, while the combined use of elemental and molecular mass spectrometry enables the accurate quantitation of structurally confirmed species. This successfully applied approach is anticipated to be a useful tool for more extensive future studies into human selenium metabolism. [ABSTRACT FROM AUTHOR]

Developing new sources of organic Se has potential benefit for animal production and human nutrition via animal-based foods enriched in Se. The objectives of this trial were to compare L-selenomethionine with another organic Se source, Se-enriched yeast (SelPlex 2300), and sodium selenite, an inorganic Se source, against a commercial control diet. The effect of source and the dosage of Se supplementation on Se in eggs and blood variables was investigated. Ten treatments were used with 18 laying hens per group. In addition to the control diet, the control diet was supplemented with L-selenomethionine, Se-enriched yeast, or sodium selenite at 0.1, 0.3, or 0.5 mg/kg of Se. The feeding trial lasted 8 wk. Birds in the different treatment groups all showed good performance. At d 0 and 56, Se and glutathione peroxidase (GPx) were analyzed in 10 blood samples per group. After supplementing the diets for 56 d, significantly higher Se levels in serum and egg contents were reached for the Se-supplemented groups compared with the control. Supplementing 0.3 and 0.5 mg/kg of L-selenomethionine or Se-enriched yeast instead of 0.1 mg/kg significantly increased the serum Se levels, whereas no significant increase was found for sodium selenite. No effect of Se source or dosage was observed on serum GPx levels. Selenium in eggs was significantly affected by dosage and source of Se. The Se supplementation level in the feed was reflected in the eggs, with the highest and lowest values for 0.5 and 0.1 mg/kg, respectively, and values in between for the 0.3 mg/kg supplementation level. A dose response was most pronounced for L-selenomethionine, followed by Se-enriched yeast, and was least when Se was added as sodium selenite. It can be concluded that Se from organic sources was more bioavailable than the inorganic Se source as evidenced by blood and egg Se levels. Within the organic Se sources, L-selenomethionine showed higher Se transfer to eggs than Se-enriched yeast. [ABSTRACT FROM AUTHOR]

Background Emerging evidence supports the view that selenoproteins are essential for maintaining bone health. Scope of review The current state of knowledge concerning selenoproteins and Se status in bone physiology and pathology is summarized. Major conclusions Antioxidant selenoproteins including glutathione peroxidase (GPx) and thioredoxin reductase (TrxR), as a whole, play a pivotal role in maintaining bone homeostasis and protecting against bone loss. GPx1, a major antioxidant enzyme in osteoclasts, is up-regulated by estrogen, an endogenous inhibitor of osteoclastogenesis. TrxR1 is an immediate early gene in response to 1α,25-dihydroxyvitamin D3, an osteoblastic differentiation agent. The combination of 1α,25-dihydroxyvitamin D3 and Se generates a synergistic elevation of TrxR activity in Se-deficient osteoblasts. Of particular concern, pleiotropic TrxR1 is implicated in promoting NFκB activation. Coincidentally, TrxR inhibitors such as curcumin and gold compounds exhibit potent osteoclastogenesis inhibitory activity. Studies in patients with the mutations of selenocysteine insertion sequence-binding protein 2, a key trans-acting factor for the co-translational insertion of selenocysteine into selenoproteins have clearly established a causal link of selenoproteins in bone development. Se transport to bone relies on selenoprotein P. Plasma selenoprotein P concentrations have been found to be positively correlated with bone mineral density in elderly women. General significance A full understanding of the role and function of selenoproteins and Se status on bone physiology and pathology may lead to effectively prevent against or modify bone diseases by using Se. [ABSTRACT FROM AUTHOR]

Abstract: This study was conducted to: (a) investigate the antagonistic interaction between selenium (Se) and mercury (Hg) in mothers and their newborns, (b) delineate the role of oxidative mechanisms induced by Hg exposure and (c) examine the protective effect of Se on Hg-induced oxidative stress and birth outcomes. Levels of Hg and Se were measured in umbilical cord blood and the placentas of 250 healthy mothers who participated in a study between 2006 and 2006 assessing prenatal exposure various pollutants. Levels of malondialdehyde (MDA) in cord and maternal blood and of 8-hydroxy-2-deoxyguanosine in urine were measured for assessing oxidative stress. Tail moment (TM) in the comet assay, as a biomarker of DNA damage was measured in samples of cord and maternal blood. The mean Se levels in umbilical cord blood (67.618±12.897μg/l) were lower than those reported in many countries, but none of the newborns had Se levels <20μg/l (the threshold limit of Keshan disease). More than 80% of the newborns, though, had Se levels below the 80μg/l needed for maximum glutathione peroxidase activity. Even though 18.6% of the newborns had levels of Hg ≥5.8μg/l (the reference dose of the Environmental Protection Agency), no relationship was observed with the biomarkers of oxidative stress. The mean placental Hg levels (0.056±0.075μg/g dry wt.) were higher than those reported for newborns with abnormal fetal development. Our study also documented significant placental transfer of Hg and Se to the fetus. The Hg/Se molar ratio in both cord blood and placental tissue was well below 1. The average amount of Se in both matrices was approximately 50-fold in molar excess over Hg. The molar excess of Se in the umbilical cord (0.843μmol/l), however, was lower than in placental tissues (13.098μmol/kg dry wt.). In further support of the relationships of Hg and Se on oxidative stress, we observed significantly lower levels of maternal MDA associated with Se levels in both cord blood and placental tissues and significantly higher TM levels associated with placental Hg in both newborns and their mothers. In contrast, Se/Hg molar ratios in placental tissues were positively associated with MDA and negatively with TM. The disproportion between Hg and Se might be influenced by the length of Hg exposure that in turn might affect Se bioavailability. Each birth anthropometric outcome was modeled as a function of Hg, Se and their interactions. After an adjustment for confounding variables, Hg in cord blood had a significantly positive rather than the expected negative association with crown-heel length. Placental Hg was associated with reduced birth height. Both associations were independent of prematurity. The status of Se in newborns was positively associated with crown-heel length and placental weight, with and without preterm births, and with birth weight, but only without preterm births. In contrast, a lower cephalization index was correlated with Se levels in cord blood, which may be an indicator of a detrimental effect on health. Our study, however, revealed associations between significantly lower levels of placental Se and several birth anthropometric measures (head circumference, birth weight and birth height) but the significance disappeared after excluding preterm births. Regression analyses generally indicated either significant or marginally significant Hg–Se antagonistic interactions that may have moderated the toxic effect of Hg on head circumference and birth weight. This finding may be due to chance or residual confounding and so may not be clinically relevant, but it may also suggest that Hg, Se and Hg–Se interactions are important factors for understanding Hg-induced adverse birth outcomes. Additional research will be necessary to evaluate the biological impact of combined metals in the assessment of fetal growth and development. [Copyright &y& Elsevier]

Abstract: Kashin–Beck disease (KBD) is a special type of endemic osteoarthritis. It has been suggested that alterations in selenium metabolism and apoptosis play a role in KBD. However, the underlying molecular mechanism remains largely unclear. We performed a microarray analysis using RNA isolated from cartilages of KBD patients and healthy controls, through Significance Analysis of Microarray (SAM) software. Functional gene networks and crucial molecules associated with differentially expressed genes were investigated via Ingenuity Pathway Analysis (IPA) and hub gene analysis. Quantitative real-time PCR was used to check the validation of chip test. We identified 52 up-regulated apoptosis-related genes and 26 down-regulated selenium-related genes between KBD and controls, and these genes associated with the “MYC-mediated apoptosis signaling pathway”. We confirmed the results from array studies with quantitative real-time PCR analysis. Our results suggest that abnormal regulation of selenium metabolism and apoptosis through the MYC mediated signaling pathway contributes to the pathogenesis of KBD, but the relationship between apoptosis gene and selenium gene was not found. [Copyright &y& Elsevier]

Abstract: Aims: Antioxidant system abnormalities have been associated with ethanol consumption. This study examines the effects of chronic ethanol consumption on oxidative balance, including selenium (Se) levels in alcoholic patients with or without liver disease, and if these measurements could be indicative of liver disease. Main methods: Serum Se levels, antioxidant enzymes' activities, malondialdehyde (MDA) and protein carbonyl (PC) were determined in three groups of patients: alcoholics without liver disease, alcoholics with liver disease, and non-alcoholics with liver disease; and in healthy volunteers. Key findings: Serum Se levels were lower in alcoholic patients and in patients affected by liver disease and especially lower in the alcoholic liver disease group. These values were correlated with the activity of glutathione peroxidase (GPx), the antioxidant selenoprotein. The antioxidant activities of the glutathione reductase (GR) and superoxide dismutase (SOD) were also lower in the three non-healthy groups. However, GR activity decreased and SOD activity increased in the non-alcoholic liver disease group versus alcoholic groups. Higher concentrations of PC in serum were found in non-healthy groups and were higher in alcoholic patients who also showed higher MDA levels. The highest MDA and PC levels were found in the alcoholic liver disease group. Significance: We conclude that serum Se levels are drastically decreased in alcoholic liver disease patients, showing that this element has a direct correlation with GPx activity, and lipid oxidation, suggesting that the serum Se/MDA ratio could be an indicator of hepatic damage caused by alcohol consumption, and pointing to Se as a possible antioxidant therapy. [Copyright &y& Elsevier]

Selenium (Se) is a bioaccumulative constituent of coal fly-ash that can disrupt reproduction of oviparous wildlife. In food webs, the greatest enrichment of Se occurs at the lowest trophic levels, making it readily bioavailable to higher consumers. However, subsequent enrichment at higher trophic levels is less pronounced, leading to mixed tendencies for Se to biomagnify. We used stable isotopes (1 5N and 13C) in claws to infer relative trophic positions and relative carbon sources, respectively, of seven turtle species near the site of a recently-remediated coal fly-ash spill. We then tested whether Se concentrations differed with relative trophic position or relative carbon source. We did not observe a strong relationship between δ15N and Se concentration. Instead, selenium concentrations decreased with increasing δ13C among species. Therefore, in an assemblage of closely-related aquatic vertebrates, relative carbon source was a better predictor of Se bioaccumulation than was relative trophic position. [Copyright &y& Elsevier]

Ethanol exposure during gestation and lactation decreases selenium (Se) intake, disrupting body Se balance and inducing oxidative stress in rat offspring. Selenium-supplemented diet (0.5 ppm) was administered to ethanol-exposed (20% v/v) dams during gestation and lactation. When the dams' pups were 21 days old, the pups' levels of the main hepatic selenoproteins glutathione peroxidase (GPx1 and GPx4) and selenoprotein P (SelP) were measured. The pups were divided into control (C), alcohol (A), control-selenium (CS), and alcohol-selenium (AS) groups. The purpose was to evaluate the effect of the selenium-supplemented diet on the levels of Se deposits present in the livers of their pups. Alcohol decreases hepatic Se deposits, GPx activity, and GPx1 expression; alcohol increases GPx4 and SelP expression. Se was measured by furnace graphite atomic absorption spectrometry, the antioxidant activity of GPx and concentration of hepatic phospholipids (PL) were determined by spectrophotometry, and the selenoprotein expressions were detected by Western blotting. Selenite treatment prevented alcohol's effects of diminishing the Se deposits, GPx activity, and GPx1 expression, while maintaining the high levels of the expression of GPx4 and SelP. These results suggest that depletion of hepatic Se levels in rat pups, caused by ethanol exposure to their dams, affects the synthesis of the 3 main hepatic selenoproteins in different ways, which is related to a decrease in GPx activity and PL concentration, and an increase in serum Se levels. Selenium supplementation to the dams increased the expression of GPx1, GPx4, and SelP in their pups. [ABSTRACT FROM AUTHOR]

Abstract: Objective(s): To evaluate selenium (Se) levels in serum and their relation with hyperandrogenism and insulin resistance (IR) in women with polycystic ovary syndrome (PCOS) and in control subjects. Study design: Women with any gynecological problem who presented to the Kahramanmaras Sutcuimam University Medical Faculty Gynecology and Obstetric Outpatient Clinic were invited to participate. Group 1 consisted of 36 cases with a diagnosis of PCOS according to the 2003 Rotterdam Consensus Criteria, and Group 2 (control group) consisted of 33 age- and BMI-matched healthy women. In all cases, serum total testosterone (tT), dihydroepiandrostenedione-sulfate (DHEAS), follicle stimulating hormone (FSH), luteinizing hormone (LH), estradiol (E2), insulin, glucose (mg/dL), total cholesterol (TC) (mg/dL), high density lipoprotein-cholesterol (HDL-C) (mg/dL), low density lipoprotein-cholesterol (LDL-C) (mg/dL), triglyceride (TG) (mg/dL) and Se levels were measured. Results: The level of FSH was significantly lower, and the levels of LH, E2, tT, and DHEAS were significantly higher in group 1 than in group 2 (p <0.05). The hirsutism score was significantly higher among PCOS women compared to the control group (p <0.05). Although insulin levels and HOMA-IR were markedly increased in the PCOS group compared to the control group, the differences were not significant (p >0.05). The plasma Se level was significantly lower in PCOS women compared to the control group (p <0.05). When we combined the all women in two groups, regarding them as one group (combined group, n =69), a negative correlation between Se and LH and tT was present (p <0.05). Conclusion(s): Our results show decreased plasma concentrations of Se and a negative correlation between Se and LH, tT in women with PCOS. These results indicate that Se may play a role in the pathogenesis of PCOS related with hyperandrogenism. [Copyright &y& Elsevier]

Abstract: It is has been hypothesized that methylselenol is a critical selenium metabolite for anticancer activity in vivo. In this study, we used a protein array which contained 112 different antibodies known to be involved in the p53 pathway to investigate the molecular targets of methylselenol in human HCT116 colon cancer cells. The array analysis indicated that methylselenol exposure changed the expression of 11 protein targets related to the regulation of cell cycle and apoptosis. Subsequently, we confirmed these proteins with the Western blotting approach, and found that methylselenol increased the expression of GADD 153 and p21 but reduced the level of c-Myc, E2F1 and Phos p38 MAP kinase. Similar to our previous report on human HCT116 colon cancer cells, methylselenol also inhibited cell growth and led to an increase in G1 and G2 fractions with a concomitant drop in S-phase in mouse colon cancer MC26 cells. When the MC26 cells were transplanted to their immune-competent Balb/c mice, methylselenol-treated MC26 cells had significantly less tumor growth potential than that of untreated MC26 cells. Taken together, our data suggest that methylselenol modulates the expression of key genes related to cell cycle and apoptosis and inhibits colon cancer cell proliferation and tumor growth. [Copyright &y& Elsevier]

The objective of this study was to determine the concentration of total selenium (Se) and the proportions of total Se comprised as selenomethionine (SeMet) and selenocysteine (SeCys) in the postmortem tissues of female pheasants (Phasianus Colchicus Torquator) offered diets that contained graded additions of selenised-enriched yeast (SY) or a single comparative dose of sodium selenite (SS). Thiobarbituric acid reactive substances (TBARS) and tissue glutathione peroxidase (GSH-Px) activity of breast (Pectoralis Major) were assessed at 0 and 5 days postmortem. A total of 216 female pheasant chicks were enrolled into the study. Twenty-four birds were euthanased at the start of the study, and samples of blood, breast muscle, leg muscle (M. Peroneus Longus and M. Gastrocnemius), heart, liver, kidney and gizzard were collected for determination of total Se. Remaining birds were blocked by live weight and randomly allocated to one of four dietary treatments (n = 48 birds/treatment) that either differed in Se source (SY v. SS) or dose (control (0.17 mg total Se/kg), SY-L and SS-L (0.3 mg/kg total Se as SY and SS, respectively) and SY-H (0.45 mg total Se/kg)). Following 42 and 91 days of treatment, 24 birds per treatment were euthanased, and samples of blood, breast muscle, leg muscle, heart, liver, kidney and gizzard were retained for determination of total Se and the proportion of total Se comprised as SeMet or SeCys. Whole blood GSH-Px activity was determined at each time point. Tissue GSH-Px activity and TBARS were determined in breast tissue at the end of the study. There were increases in both blood and tissues to the graded addition of SY to the diet (P < 0.001), but the same responses were not apparent with the blood and tissues of selenite-supplemented birds receiving a comparable dose (SY-L v. SS-L). Although there were differences between tissue types in the distribution of SeMet and SeCys, there were few differences between treatments. There were effects of treatment on erythrocyte GSH-Px activity (P = 0.012) with values being higher in treatments SY-H and SS-L when compared with the negative control and treatment SY-L. There were no effects of treatment on tissue GSH-Px activity, which is reflected in the overall lack of any treatment effects on TBARS. [ABSTRACT FROM AUTHOR]

Abstract: Objectives: Selenoprotein P (SeP) is a selenium (Se) supply protein, which is an antioxidant micronutrient considered to be vital for human health. The aim of this study was to assess the serum selenium status in patients with silicosis. Methods: We conducted a retrospective case–control study where serum samples from a total of 78 patients (males with a median age of 73.5 years old) with silicosis and 20 healthy controls (males with a median age of 72.5 years old) were assayed for Se and SeP. They underwent medical and job history taking, lung function testing, and chest radiography examinations. Levels of serum Se were measured using electrothermal atomic absorption spectrophotomerty, while levels of SeP were assessed with sandwich Enzyme Immunoassay. Spearman''s rank correlation test was carried out to evaluate the relationship between Se and SeP. The Mann–Whitney test was used to evaluate differences in serum Se and SeP between study groups. Results: The median serum Se and SeP concentrations were significantly lower in cases (74.0μg/l and 4.2mg/l, respectively) compared with controls (116.0μg/l and 5.8mg/l, respectively). In both cases and controls, serum Se was positively correlated with serum SeP (rho=0.781, p <0.001 and rho=0.768, p <0.001, respectively). Serum Se and SeP levels were significantly lower in patients classified in category four compared with those who were classified in category two or three. Conclusions: Serum Se and SeP concentrations were found to be at inadequate levels in patients with silicosis, and decreased significantly with the severity of the disease. [Copyright &y& Elsevier]

Background: Selenium is an essential trace element and as a component of selenoproteins it plays a key role as an antioxidant. We aimed to evaluate the effect of selenium supplementation during pregnancy on cord blood selenium content and lipid profile. Methods: This trial was performed on 166 eligible women who were randomized to receive 100μg of selenium, as selenium-yeast (Se group) or a placebo-yeast tablet (placebo group). Umbilical cord blood samples were collected at the time of delivery and selenium concentration and lipid profile were measured. Results: Triglyceride levels were found to be significantly higher in the Se group than in the placebo group (p =0.01). However, no significant difference in cord blood selenium was observed between the groups nor were there any significant correlations between cord blood selenium and lipid profile parameters. Conclusion: Our findings suggest that selenium supplementation in pregnant women may be associated with an increased cord-blood triglyceride level, although total cholesterol, low-density lipoprotein and high-density lipoprotein cholesterol levels did not change significantly. The clinical significance of the increased cord triglyceride concentration needs to be evaluated. [Copyright &y& Elsevier]

Abstract: Purpose: Present study aimed at determining blood selenium concentration (Se-B) in a selected population of children inhabiting industrial regions. Methods: The studies were conducted on a group of 267 children inhabiting industrial regions in Upper Silesia (Poland). Determination of Se-B was performed using hydride generation atomic absorption technique. Results: In the studied group of children mean Se-B amounted to 76.75±12.52μg/L. Only in 38.20% of studied children the estimated Se-B could be regarded as an optimal. Children with underweight (BMI<15th centile) manifested a significantly lower Se-B than children with BMI within the normal range (BMI 15–85th centile). In the entire study group of children a significant positive linear correlation was disclosed between BMI and Se-B (r =0.16, p <0.05). Regression analysis demonstrated that in the studied subgroup of children (with normal height, body mass and BMI) a higher BMI represented an independent factor of Se-B increase and a more pronounced age an independent factor of Se-B decrease. Moreover, maternal education represented an independent factor of Se-B increase in the studied group of children (with normal height, body mass and BMI). Conclusions: Se-B in the studied group children from industrial area in Upper Silesia corresponded with the lower range of blood selenium concentrations noted in recent years in other populations. A negative relationship was documented between age and Se-B and a positive relationship between BMI of a child and maternal education on one hand and Se-B of a child on the other. [Copyright &y& Elsevier]

Abstract: The inhibitory effect of oral methylseleninic acid or methylselenocysteine administration on cancer cell xenograft development in nude mice is well characterized; however, less is known about the efficacy of selenate and age on selenium chemoprevention. In this study, we tested whether selenate and duration on diets would regulate prostate cancer xenograft in nude mice. Thirty-nine homozygous NU/J nude mice were fed a selenium-deficient, Torula yeast basal diet alone (Se−) or supplemented with 0.15 (Se) or 1.0 (Se+) mg selenium/kg (as Na2SeO4) for 6 months in Experiment 1 and for 4 weeks in Experiment 2, followed by a 47-day PC-3 prostate cancer cell xenograft on the designated diet. In Experiment 1, the Se− diet enhanced the initial tumor development on days 11–17, whereas the Se+ diet suppressed tumor growth on days 35–47 in adult nude mice. Tumors grown in Se− mice were loosely packed and showed increased necrosis and inflammation as compared to those in Se and Se+ mice. In Experiment 2, dietary selenium did not affect tumor development or histopathology throughout the time course. In both experiments, postmortem plasma selenium concentrations in Se and Se+ mice were comparable and were twofold greater than those in Se− mice. Taken together, dietary selenate at nutritional and supranutritional levels differentially inhibit tumor development in adult, but not young, nude mice engrafted with PC-3 prostate cancer cells. [Copyright &y& Elsevier]

Abstract: The objective was to evaluate ovarian functionality and oxidative response in hyperandrogenism-induced polycystic ovary (PCO) and the protective effects of immunomodulator drug (IMOD), an electromagnetically-treated, selenium-based, herbal medicine. Daily oral administration of letrozole (1 mg/kg) for 21 consecutive days induced ovarian cysts in female rats. An effective dose of IMOD (30 mg/kg per day) was given intraperitoneally for 21 days. Biomarkers of ovarian function, serum concentrations of estradiol, progesterone, testosterone, and ovarian prostaglandin-E (PGE), were analyzed. To determine the role of oxidative stress (OS) in hyperandrogenism-induced PCO, concentrations of cellular lipid peroxidation (LPO), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), peroxynitrite (ONOO), and tumor necrosis factor (TNF)-α as a marker of inflammation and apoptosis were measured in serum and ovaries. Letrozole-induced PCO resulted in significant increases in concentrations of lipid peroxidation and peroxynitrite in serum and ovary, but significantly decreased superoxide dismutase, catalase, and glutathione peroxidase. Serum concentrations of testosterone and TNF-α, and ovarian prostaglandin-E were increased (P < 0.001) in animals with cysts versus control, whereas estradiol and progesterone were decreased (P < 0.01 and P < 0.001, respectively). When compared with controls, letrozole induced irregular cycles and PCO characterized by a high incidence of subcapsular ovarian cysts with a diminished granulosa cell layer, luteinized granulosa cells in the cyst wall, significantly more atretic preantral and antral follicles, and absence of CL. There were almost no intact primary, secondary, and tertiary follicles in PCO rats. All end points assessed were significantly improved by IMOD and reached close to normal levels. In conclusion, the present study provided evidence that toxic free radicals and TNF-α were involved in the pathogenesis of PCO; furthermore, IMOD prevented ovarian histopathologic, endocrine, and biochemical alterations induced by hyperandrogenism. [Copyright &y& Elsevier]

Abstract: The toxicity of selenium in fish is influenced by its chemical speciation and the exposure route. In the natural environment, selenium exposure to fish occurs primarily in the form of selenomethionine in diet. Thus, the main objective of this study was to examine the tissue-specific selenium burden and speciation in fish exposed to elevated dietary selenomethionine. Rainbow trout (Oncorhynchus mykiss) were treated with dietary selenomethionine (40μg g−1 dry mass) for 2weeks, and at the end of the exposure different tissue samples were collected to assess the tissue-specific distribution and speciation of selenium. We used synchrotron-based X-ray absorption near edge spectroscopy (XANES) to determine the selenium speciation profile. Selenomethionine, selenocysteine and selenocystine were found to be the predominant form of selenium in all of the tissues; however their relative proportion varied across different tissues. In general, the organs primarily involved in selenium handling in fish (e.g., liver, kidney) accumulated a higher percentage of selenocystine. We also found that dietary selenomethionine exposure resulted into a marked increase in selenium burden of all major tissues in fish including the brain. Collectively, our findings provide new insights into the tissue-specific distribution and speciation of selenium in fish exposed to selenomethionine via diet. [Copyright &y& Elsevier]

Abstract: Increasing emissions of anthropogenic mercury represents a growing concern to the health of high trophic level marine mammals. In its organic form, this metal bioaccumulates, and can be toxic to several physiological endpoints, including the immune system. In this study, we (1) evaluated the effects of inorganic mercury (mercuric chloride, HgCl2) and organic mercury (methylmercuric chloride, MeHgCl) on the in vitro function of lymphocytes isolated from the peripheral blood of beluga whales (Delphinapterus leucas); (2) characterized the potential protective effects of sodium selenite (Na2SeO3) on cell proliferation of HgCl2 or MeHgCl-treated beluga whale lymphocytes; and (3) compared these dose-dependent effects to measurements of blood Hg in samples collected from traditionally harvested beluga whales in the western Canadian Arctic. Lymphocyte proliferative responses were reduced following exposure to 1μM of HgCl2 and 0.33μM of MeHgCl. Decreased intracellular thiol levels were observed at 10μM of HgCl2 and 0.33μM of MeHgCl. Metallothionein induction was noted at 0.33μM of MeHgCl. Concurrent exposure of Se provided a degree of protection against the highest concentrations of inorganic Hg (3.33 and 10μM) or organic Hg (10μM) for T-lymphocytes. This in vitro protection of Se against Hg toxicity to lymphocytes may contribute to the in vivo protection in beluga whales exposed to high Hg concentrations. Current Hg levels in free-ranging beluga whales from the Arctic fall into the range of exposures which elicited effects on lymphocytes in our study, highlighting the potential for effects on host resistance to disease. The implications of a changing Arctic climate on Hg fate in beluga food webs and the consequences for the health of beluga whales remain pressing research needs. [Copyright &y& Elsevier]

Abstract: The biological function of selenium (Se) is determined by its form and concentration. Selenium is an essential micronutrient for all vertebrates, however, at environmental levels, it is a potent toxin. In the San Francisco Bay-Delta, Se pollution threatens top predatory fish, including white sturgeon. A multi-compartmental Bayesian hierarchical model was developed to estimate the fractional rates of absorption, disposition, and elimination of selenocompounds, in white sturgeon, from tissue measurements obtained in a previous study (). This modeling methodology allows for a population based approach to estimate kinetic physiological parameters in white sturgeon. Briefly, thirty juvenile white sturgeon (five per treatment) were orally intubated with a control (no selenium) or a single dose of Se (500μgSe/kgbody weight) in the form of one inorganic (Selenite) or four organic selenocompounds: selenocystine (SeCys), l-selenomethionine (SeMet), Se-methylseleno-l-cysteine (MSeCys), or selenoyeast (SeYeast). Blood and urine Se were measured at intervals throughout the 48h post intubation period and eight tissues were sampled at 48h. The model is composed of four state variables, conceptually the gut (Q 1), blood (Q 2), and tissue (Q 3); and urine (Q 0), all in units of μgSe. Six kinetics parameters were estimated: the fractional rates [1/h] of absorption, tissue disposition, tissue release, and urinary elimination (k 12, k 23, k 32, and k 20), the proportion of the absorbed dose eliminated through the urine (f 20), and the distribution blood volume (V; percent body weight, BW). The parameter k 12 was higher in sturgeon given the organic Se forms, in the descending order of MSeCys>SeMet>SeCys>Selenite>SeYeast. The parameters k 23 and k 32 followed similar patterns, and f 20 was lowest in fish given MSeCys. Selenium form did not affect k 20 or V. The parameter differences observed can be attributed to the different mechanisms of transmucosal transport, metabolic reduction, and storage of the Se forms, which, in general, appear to be similar to that in mammals. We have demonstrated that the Bayesian approach is a powerful tool for integrating quantitative information from a study with sparse blood and urinary measurements and tissue concentrations from a single time point, while providing a full characterization of parameter variability. The model permits the quantitative mechanistic interpretation and predictions of Se absorption, disposition, and elimination processes. Furthermore, the model represents a first step towards population based physiological toxicokinetic modeling of Se in white sturgeon. [Copyright &y& Elsevier]

Abstract: Selenium (Se) is an essential micronutrient for all vertebrates, however, at environmental relevant levels, it is a potent toxin. In the San Francisco Bay-Delta, white sturgeon, an ancient Chondrostean fish of high ecological and economic value, is at risk to Se exposure. The present study is the first to examine the uptake, distribution, and excretion of various selenocompounds in white sturgeon. A combined technique of stomach intubation, dorsal aorta cannulation, and urinary catheterization was utilized, in this study, to characterize the short-term effects of Se in the forms of sodium-selenate (Selenate), sodium-selenite (Selenite), selenocystine (SeCys), l-selenomethionine (SeMet), Se-methylseleno-l-cysteine (MSeCys), and selenoyeast (SeYeast). An ecologically relevant dose of Se (∼500μg/kg body weight) was intubated into groups of 5 juvenile white sturgeon. Blood and urine samples were repeatedly collected over the 48h post intubation period and fish were sacrificed for Se tissue concentration and distribution at 48h. The tissue concentration and distribution, blood concentrations, and urinary elimination of Se significantly differ (p ≤0.05) among forms. In general, organic selenocompounds maintain higher blood concentrations, with SeMeCys maintaining the highest area under the curve (66.3±8.7 and 9.3±1.0μgh/ml) and maximum Se concentration in blood (2.3±0.2 and 0.4±0.2μg/ml) in both the protein and non-protein bound fractions, respectively. Selenate, however, did not result in significant increase of Se concentration, compared with the control, in the protein-bound blood fraction. Regardless of source, Se is preferentially distributed into metabolically active tissues, with the SeMet treated fish achieving the highest concentration in most tissues. In contrast, Selenite has very similar blood concentrations and tissue distribution profile to SeCys and SeYeast. From blood and tissue Se concentrations, Selenate is not stored in blood, but taken up rapidly by the liver and white muscle. Urinary elimination of Se is form dependent and peaks between 3 and 12h post intubation. A basic understanding of the overall Se absorption, distribution, and elimination is provided through monitoring tissue Se concentrations, however, conclusions regarding to the dynamics and the specific processes of Se metabolism can only be inferred, in the absence of kinetic information. [Copyright &y& Elsevier]

Abstract: It was investigated whether the ability of zinc (Zn) to prevent cadmium (Cd)-induced lipid peroxidation may be connected with its impact on glutathione peroxidase (GPx) activity and selenium (Se) concentration. GPx and Se were determined in the serum, liver and kidney of the rats that received Cd (5 or 50mg/L) or/and Zn (30mg/L) in drinking water for 6 months in whose the protective Zn impact was noted (Rogalska J, Brzóska MM, Roszczenko A, Moniuszko-Jakoniuk J. Enhanced zinc consumption prevents cadmium-induced alterations in lipid metabolism in male rats. Chem Biol Interact 2009;177:142–52). Moreover, dependences between these parameters, and indices of lipid peroxidation (F2-isoprostane, lipid peroxides, oxidized low density lipoprotein cholesterol) as well as concentrations of Cd and Zn were estimated. The supplementation with Zn during the exposure to 5mg Cd/L entirely antagonized the Cd-induced increase in GPx activity and Se concentration in the liver and kidney, but not in the serum. Zn administration during the treatment with 50mg Cd/L totally or partially prevented from the Cd-caused decrease in GPx activity and Se concentration in the serum, liver and kidney. At the higher level of Cd exposure, GPx activity in the serum and tissues positively correlated with Se concentration. Moreover, numerous correlations were noted between GPx and/or Se and the indices of lipid peroxidation. The results indicate that the protective impact of Zn against the Cd-induced lipid peroxidation during the relatively high exposure might be connected with its beneficial influence on Se concentration and GPx activity in the serum and tissues, whereas this bioelement influence at the moderate exposure seems to be independent of GPx and Se. [Copyright &y& Elsevier]