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Background: Oxidative stress and inflammation are considered to be important pathways leading to particulate matter (PM)-associated disease. In this exploratory study, we examined the effects of metals and oxidative potential (OP) in urban PM on biomarkers of systemic inflammation, oxidative stress and neural function., Methods: Fifty-three healthy non-smoking volunteers (mean age 28 years, twenty-eight females) were exposed to coarse (2.5-10 μm, mean 213 μg/m 3 ), fine (0.15-2.5 μm, 238 μg/m 3 ), and/or ultrafine concentrated ambient PM (<0.3 μm, 136 μg/m 3 ). Exposures lasted 130 min, separated by ≥2 weeks. Metal concentrations and OP (measured by ascorbate and glutathione depletion in synthetic airway fluid) in PM were analyzed. Blood and urine samples were collected pre-exposure, and 1-h and 21-h post exposure for assessment of biomarkers. We used mixed-regression models to analyze associations adjusting for PM size and mass concentration., Results: Results for metals were expressed as change (%) from daily pre-exposure biomarker levels after exposure to a metal at a level equivalent to the mean concentration. Exposure to various metals (silver, aluminum, barium, copper, iron, potassium, lithium, nickel, tin, and/or vanadium) was significantly associated with increased levels of various blood or urinary biomarkers. For example, the blood inflammatory marker vascular endothelia growth factor (VEGF) increased 5.3% (95% confidence interval: 0.3%, 10.2%) 1-h post exposure to nickel; the traumatic brain injury marker ubiquitin C-terminal hydrolase L1 (UCHL1) increased 11% (1.2%, 21%) and 14% (0.3%, 29%) 1-h and 21-h post exposure to barium, respectively; and the systemic stress marker cortisol increased 1.5% (0%, 2.9%) and 1.5% (0.5%, 2.8%) 1-h and 21-h post exposure to silver, respectively. Urinary DNA oxidation marker 8‑hydroxy‑deoxy‑guanosine increased 14% (6.4%, 21%) 1-h post exposure to copper; urinary neural marker vanillylmandelic acid increased 29% (3%, 54%) 1-h post exposure to aluminum; and urinary cortisol increased 88% (0.9%, 176%) 1-h post exposure to vanadium. Results for OP were expressed as change (%) from daily pre-exposure biomarker levels after exposure to ascorbate-related OP at a level equivalent to the mean concentration, or for exposure to glutathione-related OP at a level above the limit of detection. Exposure to ascorbate- or glutathione-related OP was significantly associated with increased inflammatory and neural biomarkers including interleukin-6, VEGF, UCHL1, and S100 calcium-binding protein B in blood, and malondialdehyde and 8-hydroxy-deoxy-guanosine in urine. For example, UCHL1 increased 9.4% (1.8%, 17%) in blood 21-h post exposure to ascorbate-related OP, while urinary malondialdehyde increased 19% (3.6%, 35%) and 8-hydroxy-deoxy-guanosine increased 24% (2.9%, 48%) 21-h post exposure to ascorbate- and glutathione-related OP, respectively., Conclusion: Our results from this exploratory study suggest that metal constituents and OP in ambient PM may influence biomarker levels associated with systemic inflammation, oxidative stress, perturbations of neural function, and systemic physiological stress., (Crown Copyright © 2018. Published by Elsevier Ltd. All rights reserved.)

Background: Iodine is a part of thyroid hormones and has been reported to act directly as an antioxidant or induce indirectly antioxidant enzymes. This study aimed to assess the urinary iodine concentration and its relationship between the antioxidant and oxidative stress capacity in healthy school-aged children., Methods: In total, 196 students from five primary schools, randomly selected between 9 and 12 years (mean age: 10.2±1.2 years), were enrolled in the study. Urinary iodine levels were measured by spectrophotometry with the Sandell-Kolthoff reaction. Total antioxidant status (TAS) and total oxidant status (TOS) were analysed from urine samples. The ratio of TOS to TAS was regarded as an oxidative stress index (OSI), an indicator of the degree of oxidative status., Results: Fifty-four percentage (107) of the children had iodine deficiency (ID) and the majority of them (30%) had mild ID. There was no severe-ID child in the population (<20 μg/L). Urine TAS levels were significantly lower in the moderate-ID group than in the mild-ID group (6.5±4.1 vs. 11.3±4.1 mmol, p<0.001) and the iodine-sufficient group (11.0±5.3 μmol, p<0.001). TOS levels and OSI were found higher in the moderate-ID group than in the mild-ID group (4.8±2.1 vs. 3.7±2.1 μmol, p<0.001) and the iodine-sufficient group (4.8±2.1 vs. 3.4±2.5 mmol, p<0.001). In the moderate-ID group, low urine iodine levels exhibited significant negative correlations with OSI (r=-0.660) and TOS (r=-0.248) and a positive correlation with TAS (r=0.475)., Conclusions: We found that children with moderate ID were exposed to more oxidative burden than children with mild ID or iodine sufficiency. Increased systemic oxidative stress induced by moderate ID could cause development of ID-related complications and diseases. Iodine supplementation could have a beneficial role in the prevention of oxidative stress.

Objective: The objective of this study is to assess the association of blood and urinary oxidative stress parameters and inflammatory markers in women with gestational hypertension and preeclampsia., Design and Methods: Malondialdehyde, protein bound sialic acid and C-reactive protein were estimated in serum and urine of pregnant women diagnosed with preeclampsia (n=30) and gestational hypertension (n=30) and the results were compared with 30 normal pregnant women., Results: Whole blood glutathione level was reduced, and malondialdehyde and C-reactive protein levels were significantly higher and correlated with each other in preeclampsia (p<0.05). Urinary malondialdehyde significantly correlated with urinary protein bound sialic acid in preeclampsia (r=0.412; p=0.02). Receiver operating curve analysis of serum protein bound sialic acid and serum malondialdehyde showed reasonable cutoff values for the differential diagnosis of preeclampsia., Conclusions: Oxidative stress and inflammatory response are greater in women with preeclampsia in comparison to pregnant women with gestational hypertension and there is an association between oxidative stress and inflammatory response., (Copyright © 2012 The Canadian Society of Clinical Chemists. Published by Elsevier Inc. All rights reserved.)

Six separate methods to detect oxidants in urine were developed. The presence of the oxidants was established by initial oxidation of ferrous to ferric ion and detecting the ferric by chromogenic oxidation or complex formation. The reagents for chromogenic oxidation were N,N-dimethylamoino-1,4-phenylenediamine (DMPDA), 2,2'-azino-bis(3-ethylbenzthiazoline-6-sulfonic acid (ABTS), and 2-amino-p-cresol (APC), and the reagents for the chromogenic complex were xylenol orange (XO), 8-hydroxy-7-iodo-5-quinolinesulfonic acid (HIQSA), and 4,5-dihydroxy-1,3-benzene-di-sulfonic acid (HBSA). All methods showed comparable results when tested for ferric, chromate, permanganate, oxychloride, hydrogen peroxide, oxone, tert-butylhydroperoxide, and cumenehydroperoxide at a concentration of 1.0 mmol/L in water (CV < 7%). The nitrite results are comparable only with DMPDA and APC. Periodate responded to the highest oxidation number (ON = 8) by chromogenic oxidation but lowest (ON = 2) by the chromogenic complex. The iodate responded only to the chromogenic oxidation with ON = 6. The linearity of the procedures was established by chromate in water. The linear concentrations were 0.09-12.00 mE/L for DMPDA, ABTS, APC, and HBSA and 0.09-6.00 mE/L for XO and HIQSA. In all methods, the correlation coefficients were > or = 0.9991 and precisions were within +/- 5.6%. The methods were used to test oxidants in 238 urine specimens. The chromate at 3.0 mE/L in water was used as standard. The correlation coefficients of 0.9600-0.9853 and the ANOVA test (F = 0.90, F(critical) = 2.22 at P(0.48)) indicated that the methods correlated well. The median concentration of oxidants in the specimens was 0.21 mE/L with an average and standard deviation of 0.62 +/- 1.19 (range 0.04-8.83 mE/L). When Grubbs' statistical test was applied to the specimen results, no specimen was found to be outlier or could be considered as adulterated. The Grubbs' test also revealed that the threshold concentration to identify urine adulteration was 29 mE/L at confidence level of 99%.

Objective: We investigated whether solutions of enteral vitamin supplementation are involved in the generation of peroxides and whether that contamination is biologically significant., Methods: Peroxide contents of oral multivitamin preparations were measured over 3 wk after the initial opening of the containers. In selected premature infants (younger than 35 wk gestation), urinary peroxides were measured after initiating oral multivitamin supplementation., Results: Peroxides in multivitamin solutions for enteral use are predominantly organic peroxides because they resist catalase. After the initial opening of the containers, there was a two-fold increase in total peroxides levels (P < 0.05) even in the preparation without riboflavin, a catalyst for the generation of peroxides. Initiation of oral vitamin supplementation was associated with increased (P < 0.05) urine peroxide levels. The high organic peroxide load did not correlate with its urinary excretion, mostly in the form of H(2)O(2). The excretion of H(2)O(2) corresponded to its oral intake from the multivitamin solution., Conclusions: Compared with parenteral multivitamin solutions, the enteral preparations contained higher organic peroxide levels starting with the initial opening of the bottles. The increased urinary excretion of H(2)O(2) after enteral multivitamin supplementation suggested a systemic diffusion of peroxides or of components of the multivitamin preparation responsible for the generation of peroxides. This oxidant load was not quenched by the immature antioxidant defenses of premature infants.

An increased urinary excretion of trimethylamine and its N-oxide were observed in man following the oral intake (15 mmol) of choline (63% dose as trimethylamine and its N-oxide), D,L-carnitine (31% dose) and trimethylamine N-oxide (78% dose). Similar ingestion of betaine, creatinine or lecithin failed to elicit any significant increases. Of 46 different foods investigated, only fish and other sea-products gave rise to significant increases in urinary trimethylamine and N-oxide. Ingestion of fruits, vegetables, cereal and dairy produce, and meats had no measurable effects. Reasons for the apparent lack of trimethylamine provision by foods previously thought to be precursors are given and the role of gut microflora highlighted.

Background: Trimethylaminuia is an unusual observation, often termed fish odor syndrome. The condition results from reduced ability to oxidize trimethylamine (TMA), which has a fishy odor, into odorless trimethylamine N-oxide (TMAO)., Method: Proton nuclear magnetic resonance spectroscopy (MRS) was used as a simple and rapid method to detect TMA and TMAO in the same urine sample without pretreatment. Subjects were considered to have deficient N-oxidation of TMA if the TMAO/TMA ratio was greater than 80 p. 100 (heterozygous) or 65 p. 100 (homozygous)., Discussion: Direct proton RRS analysis of urine is well suited for diagnosis of fish odor syndrome. It can be used to detect heterozygous patients and also provides an easily implemented follow-up tool.