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Oxidative stress is an important component of slow pathological inflammation in metabolic diseases and chronic periodontitis. Periodontal diseases are interrelated with somatic pathology. This results in both local and systemic inflammatory reactions, which increases the risk of the onset and progression of somatic diseases. Psychological stress associated with oxidative stress with increased production of oxidants and oxidative damage is an important factor in the etiology of both periodontitis and metabolic disorders. Objective — to analyze the possible bond between chronic periodontitis, 8‑hydroxydeoxyguanosine (8‑OHdG), as a biomarker of oxidative stress, and cortisol in persons with metabolic‑associated diseases. Materials and methods. 68 people were surveyed, of which 47 had metabolically ‑associated diseases that were diagnosed according to domestic and international criteria. The control group consisted of systematically healthy people, representative by age and article that did not receive dental therapeutic and preventive measures for the last 6 months. The diagnosis of «chronic periodontitis» was carried out in accordance with existing recommendations provided at World Workshop on the Classification of Periodontal and Peri­Implant Diseases and Conditions (2017). The concentration of 8‑OHdG in plasma and the level of saliva cortisol were measured by the immunoenzyme method according to the manufacturer’s instructions. The arithmetic mean, standard error, and Student’s t‑test were calculated to compare the characteristics. Pearson’s correlation test was used to identify the relationship between the indicators. Results. Each of the groups had patients who had a healthy periodontium and those who had chronic periodontitis. The 8‑OHdG level in the main group was much higher (p<0.001) than in the control group, and the difference in the concentration of 8‑OHdG was also observed between those patients who had periodontal disease and those who had a&

Highlights: Oxidative markers 8-Hydroxydeoxyguanosine and Nitric Oxide was found high in hemodialysis and non-hemodialysis chronic kidney disease patients. There is no correlation between 8-Hydroxydeoxyguanosine and Nitric Oxide in hemodialysis and non-hemodialysis chronic kidney disease patients. Abstract: Oxidative stress is essential to chronic kidney disease (CKD). Several markers include 8-Hydroxydeoxyguanosine (8-OHdG) and Nitric Oxide (NO). Reactive oxygen species (ROS) and Reactive Nitrogen Species (RNS) increased in CKD and had a role in renal impairment progressivity. There are some controversies regarding oxidative markers in CKD patients in several studies. This study aimed to understand oxidative markers 8-OHdG and NO and explained the correlation of both markers in hemodialysis and non-hemodialysis CKD patients. Twenty hemodialysis patients and forty-nine non-hemodialysis patients were enrolled in this cross-sectional study. Urine patients were collected to measure 8-OHdG using the enzyme-linked immunoassay (ELISA) method, and NO was measured from serum patients using the Griss Saltzman method. Based on Bivariate Pearson analysis, there was no significant correlation between 8-OHdG urine and total NO serum in the hemodialysis group (p= 0,510, p>0.05) and in the non-hemodialysis group (p= 0.801, p>0,05). In this study, DNA oxidative marker, 8-OHdG, was not correlated with NO in CKD patients.

Highlights: Oxidative markers 8-Hydroxydeoxyguanosine and Nitric Oxide was found high in hemodialysis and non-hemodialysis chronic kidney disease patients. There is no correlation between 8-Hydroxydeoxyguanosine and Nitric Oxide in hemodialysis and non-hemodialysis chronic kidney disease patients. Abstract: Oxidative stress is essential to chronic kidney disease (CKD). Several markers include 8-Hydroxydeoxyguanosine (8-OHdG) and Nitric Oxide (NO). Reactive oxygen species (ROS) and Reactive Nitrogen Species (RNS) increased in CKD and had a role in renal impairment progressivity. There are some controversies regarding oxidative markers in CKD patients in several studies. This study aimed to understand oxidative markers 8-OHdG and NO and explained the correlation of both markers in hemodialysis and non-hemodialysis CKD patients. Twenty hemodialysis patients and forty-nine non-hemodialysis patients were enrolled in this cross-sectional study. Urine patients were collected to measure 8-OHdG using the enzyme-linked immunoassay (ELISA) method, and NO was measured from serum patients using the Griss Saltzman method. Based on Bivariate Pearson analysis, there was no significant correlation between 8-OHdG urine and total NO serum in the hemodialysis group (p= 0,510, p>0.05) and in the non-hemodialysis group (p= 0.801, p>0,05). In this study, DNA oxidative marker, 8-OHdG, was not correlated with NO in CKD patients.

Background/Aim: Diffuse large B‐cell lymphoma (DLBCL) is an aggressive malignancy where antioxidant enzyme peroxiredoxin 6 (Prx6) has previously been associated with adverse outcomes. Its systemic effects in DLBCL are unknown. Materials and methods: This study included 53 patients with DLBCL, five patients with primary central nervous system lymphoma (PCNSL) and 20 healthy controls. The expression of Prx6 was evaluated immunohistochemically in DLBCL tissue samples and compared to its expression in blood serum. Results: Prx6 expression was the highest in healthy controls, followed by DLBCL patients and PCNSL patients. Febrile neutropenic infection after the first treatment course was associated with low pre-treatment Prx6 serum levels (<14 ng/ml) (p=0.025, OR=8.615, 95% confidence interval=1.032‐71.933). Serum levels of Prx6 recovered after treatment (p=0.006). Conclusion: Patients with low Prx6 levels might be more prone to treatment‐related adverse effects through elevated levels of oxidative stress.

The senescence- accelerated mouse prone 8 (SAMP8) is a well- characterized animal model of senescence that shows early age- related neurodegeneration with impairment in learning and memory skills when compared with control senescence- resistant mice (SAMR1). In the current study, we investigated whether such impairment could be partly due to changes in mitochondrial DNA (mtDNA) repair capacity and mitochondrial DNA damage in the brain of SAMP8 mice. Besides we studied whether these potential changes were related to modifications in two major processes likely involved in aging and neurodegeneration: apoptosis and inflammation. We observed that the specific activity of one of the main mtDNA repair enzymes, the mitochondrial APE1, showed an age- related reduction in SAMP8 animals, while in SAMR1 mice mitochondrial APE1 increased with age. The reduction in mtAPE1 activity in SAMP8 animals was associated with increased levels of the DNA oxidative damage marker 8oxodG in mtDNA. Our results also indicate that these changes were related to a premature increase in apoptotic events and inflammation in the brain of SAMP8 mice when compared to SAMR1 counterparts. We suggest that the premature neurodegenerative phenotype observed in SAMP8 animals might be due, at least in part, to changes in the processing of mtDNA oxidative damage, which would lead to enhancement of apoptotic and inflammatory processes., Universidad Complutense / Comunidad de Madrid, Depto. de Genética, Fisiología y Microbiología, Fac. de Ciencias Biológicas, TRUE, pub

The senescence- accelerated mouse prone 8 (SAMP8) is a well- characterized animal model of senescence that shows early age- related neurodegeneration with impairment in learning and memory skills when compared with control senescence- resistant mice (SAMR1). In the current study, we investigated whether such impairment could be partly due to changes in mitochondrial DNA (mtDNA) repair capacity and mitochondrial DNA damage in the brain of SAMP8 mice. Besides we studied whether these potential changes were related to modifications in two major processes likely involved in aging and neurodegeneration: apoptosis and inflammation. We observed that the specific activity of one of the main mtDNA repair enzymes, the mitochondrial APE1, showed an age- related reduction in SAMP8 animals, while in SAMR1 mice mitochondrial APE1 increased with age. The reduction in mtAPE1 activity in SAMP8 animals was associated with increased levels of the DNA oxidative damage marker 8oxodG in mtDNA. Our results also indicate that these changes were related to a premature increase in apoptotic events and inflammation in the brain of SAMP8 mice when compared to SAMR1 counterparts. We suggest that the premature neurodegenerative phenotype observed in SAMP8 animals might be due, at least in part, to changes in the processing of mtDNA oxidative damage, which would lead to enhancement of apoptotic and inflammatory processes., Universidad Complutense / Comunidad de Madrid, Depto. de Genética, Fisiología y Microbiología, Fac. de Ciencias Biológicas, TRUE, pub

Background: Oxidative stress and redox-regulating enzymes may potentially accelerate pancreatic carcinogenesis and also affect chemoresistance. Recently major antioxidant response regulator NF-E2-related factor 2 (Nrf2) has been linked to poor prognosis in pancreatic cancer. Nrf2 activity is strictly regulated by oxidative stress sensor Kelch-like ECH-associated protein 1 (Keap1). Oxidative DNA damage can be estimated e.g. by 8-hydroxy-2′-deoxyguanosine (8-OHdG) expression. The aim of this study was to evaluate the expression and possible prognostic role of Keap1 and 8-OHdG in pancreatic cancer. Methods: We assessed immunohistochemically the expression of 8-OHdG and Keap1 in precisely characterized material of 69 pancreatic adenocarcinoma patients. Results: Nuclear 8-OHdG associated with cytoplasmic Keap1 expression (p = 0.031) and was overexpressed in patients with smaller tumors (p = 0.016) and in tumors without lymph node involvement (p = 0.051). Cytoplasmic 8-OHdG expression associated with higher differentiation (p = 0.023). Cytoplasmic Keap1 immunostaining associated with N0-staging (p = 0.0009) and the absence of distant metastases (p = 0.018). Membranous Keap1 associated with longer relapse-free survival (p = 0.041) and pancreatic cancer-specific survival (median survival 14 vs. 32 months; p = 0.029) and was in multivariate analysis an independent prognostic factor of pancreatic cancer-related death (HR 2.66, 95%CI 1.23–5.75). Conclusions: Oxidative stress and main redox regulators may participate in pancreatic carcinogenesis and Keap1 appears as a promising prognostic factor in pancreatic cancer. Future studies should also concentrate on potential link between redox regulation and chemoresistance in pancreatic cancer.

Cancer is the leading cause of death worldwide. Despite the significant research effort, underlying mechanisms of carcinogenic processes are still poorly understood. In recent decades, a group of extremely reactive oxygen metabolites, reactive oxygen species (ROS), have been linked closely to carcinogenesis. Levels of ROS are constantly controlled by antioxidants to ensure stable redox balance in our cells. An aberrant cellular redox balance is thought to be connected to carcinogenesis by inflicting damage to cellular macromolecules and disturbing normal cellular signalling. In this work, the role of ROS in carcinogenesis was studied by observing the ROS-derived DNA damage marker 8-hydroxydeoxyguanosine (8-OHdG) in breast cancer and endometriosis-associated ovarian cancer. This marker was also measured in connection with endometriosis and PCOS to study the early stages of the carcinogenic process. In addition, peroxiredoxin antioxidant enzymes were studied in endometriosis-associated ovarian cancer to explore their impact on the carcinogenic process and relationship with ROS-derived DNA damage. There seems to be a decreasing trend in the expression of 8-OHdG in the development of breast cancer and endometriosis-associated ovarian cancer. In breast cancer, low levels of 8-OHdG in serum and in tumour tissue were found to be associated with more aggressive disease. In endometriosis-associated ovarian cancer, 8-OHdG and Prx II expressions in tissue decreased with malignant transformation from benign endometriosis tissue to ovarian cancer. Patients with PCOS were found to have lower levels of 8-OHdG in serum compared with healthy controls and metformin treatment further decreased 8-OHdG levels in obese patients. These results, together with observations is previous studies indicate that in breast cancer and endometriosis-associated ovarian cancer, a high level of ROS-derived DNA damage could be significant factor in the initiation stage of carcinogenesis, wherea, Tiivistelmä Syöpä on nykyisin maailman yleisin kuolinsyy. Vaikka syöpätutkimukseen kohdistetaan maailmanlaajuisesti huomattavia resursseja, syövän kehittymisen perimmäinen syy on edelleen heikosti tunnettu. Yhä kasvavan todistusaineiston perusteella happiradikaalien epäillään liittyvän läheisesti syövän kehittymiseen. Nämä erittäin reaktiiviset hapen aineenvaihduntatuotteet ovat välttämättömiä solujemme normaalille toiminnalle, mutta liian suurina määrinä ne voivat vaurioittaa solun rakenteita ja häiritä solun normaalia viestintää. Solut sisältävät useita antioksidantteja, joiden tärkeimpänä tehtävänä on kontrolloida happiradikaalien määrää ja näin ylläpitää solun hapetus–pelkistys-tasapaino. Tässä väitöskirjatutkimuksessa tutkittiin happiradikaalien yhteyttä syövän kehittymiseen tarkastelemalla niiden aiheuttaman DNA-vaurion merkkiainetta, 8-hydroksideoksiguanosiinia (8-OHdG), rintasyövässä ja endometrioosiin liittyvässä munasarjasyövässä sekä peroksiredoksiiniperheen antioksidanttientsyymejä endometrioosiin liittyvässä munasarjasyövässä. 8-OHdG:n avulla selvitettiin myös munasarjojen monirakkulaoireyhtymän (PCOS) ja endometrioosin yhteyttä syövän kehittymiseen. Lisäksi tutkittiin metformiinin vaikutusta happiradikaalien aiheuttamaan DNA-vaurioon. Väitöskirjatutkimuksen tulosten perusteella 8-OHdG:n määrä vähentyy rintasyövän edetessä ja endometrioosiin liittyvän munasarjasyövän kehittyessä. Matalat 8-OHdG-tasot syöpäkudoksessa ja verinäytteissä ovat yhteydessä aggressiivisempaan taudinkuvaan rintasyövässä. Endometrioosiin liittyvässä munasarjasyövässä kudoksen ilmentämä 8-OHdG ja Prx II vähentyi asteittain siirryttäessä hyvänlaatuisesta endometrioosista munasarjasyöpään. Munasarjojen monirakkulaoireyhtymässä potilaiden verinäytteiden 8-OHdG-tasot olivat merkittävästi matalammat terveisiin verrokkeihin verrattuna. Korkeilla happiradikaalipitoisuuksilla ja niistä aiheutuvalla DNA-vauriolla on väitöskirjatutkimuksen tulosten perusteella tärkeä rooli syövän syntyvaihe

[EN] The effect of a product made of dehydrated apples enriched with mandarin juice by vacuum impregnation on markers of oxidative stress (plasma antioxidant capacity, carbonyl groups (CGs), 8-hydroxydeoxyguanosine (8OHdG) and alpha-tocopherol) was tested in rats. Six groups of animals were studied: one group was fed a standard diet; two groups were supplemented with dehydrated apple either impregnated or not with mandarin juice throughout 28 days; and three groups (one unsupplemented and two supplemented) were additionally treated with tamoxifen (TAM) for 21 days used for induction of oxidative stress. The rats treated with TAM showed an increase in aminotransferases, CGs and 8OHdG. All of these effects were significantly decreased in the animals after apple snack consumption; the addition of mandarin juice into the apple mainly accounts for increased levels of alpha-tocopherol in plasma and liver. These findings suggest that the food product have a protective action against oxidative stress induced by TAM in rats.

[EN] The effect of a product made of dehydrated apples enriched with mandarin juice by vacuum impregnation on markers of oxidative stress (plasma antioxidant capacity, carbonyl groups (CGs), 8-hydroxydeoxyguanosine (8OHdG) and alpha-tocopherol) was tested in rats. Six groups of animals were studied: one group was fed a standard diet; two groups were supplemented with dehydrated apple either impregnated or not with mandarin juice throughout 28 days; and three groups (one unsupplemented and two supplemented) were additionally treated with tamoxifen (TAM) for 21 days used for induction of oxidative stress. The rats treated with TAM showed an increase in aminotransferases, CGs and 8OHdG. All of these effects were significantly decreased in the animals after apple snack consumption; the addition of mandarin juice into the apple mainly accounts for increased levels of alpha-tocopherol in plasma and liver. These findings suggest that the food product have a protective action against oxidative stress induced by TAM in rats.

Mortality studies have shown that, in the past, lung cancer occurred after exposure to mixtures of cobalt metal and metallic carbide particles, the main constituents of hard metals, but apparently not when exposure was to cobalt alone. The major objective of this biomonitoring study was to assess genotoxic effects as a measure for carcinogenic risk in workers From cobalt refineries and hard metal plants currently exposed to the threshold limit value/time-weighted average (TLV-TWA) for cobalt-containing dust. The study comprised three groups of workers: 35 workers exposed to cobalt dust From three refineries, 29 workers exposed to hard metal dust from two producing plants, and 35 matched control subjects recruited from the respective plants. The study design integrated complementary methodologies to assess biomarkers of effects that represent both initial DNA damage (8-hydroxydeoxyguanosine [8-OHdG] in urine and comet assay on lymphocytes) and definitive chromosome breakage/loss (micronuclei in lymphocytes). Cobalt and cotinine were determined in urine as a measure for cobalt exposure and recent smoking, respectively. No significant increase of genotoxic effects was detected in workers exposed to cobalt-containing dust as compared to controls. No difference in any genotoxicity biomarker was Found between workers exposed to cobalt and hard metal dusts. Multiple regression analysis indicated that workers who smoked and were exposed to hard metal dusts had elevated 8-OHdG and micronuclei valves. Because this observation is in line with a previous epidemiological study of an increased risk of dying from lung cancer in workers from the hard metal industry who smoked, it is concluded that this specific occupational group needs closer medical surveillance.. (C) 2000 Wiley-Liss, Inc.

Conjugated linoleic acid (CLA) is a naturally occurring component of the food supply that has been shown to inhibit the development of experimentally-induced breast cancer. One reported explanation for this protective activity against carcinogenesis is that ClA is an antioxidant. Studies were completed during the current reporting period that indicate that CIA does reduce lipid peroxidation levels measured as malondialdehyde in mammary tissue, which is predominantly comprised of neutral lipid, but not in liver membrane phospholipid. CIA supplementation failed to alter tissue concentrations of 8-hydroxydeoxyguanosine (8-HdG), an indicator of oxidative DNA base damage, irrespective of its effect on tissue malondialdehyde levels. These observations were made under conditions of constitutive as well as induced oxidative stress. Collectively, these data indicate that the cancer inhibitory activity of CIA is unlikely to be due to its antioxidant activity. Given these observations we are now focusing our efforts on determining the effects of CIA on mammary gland development and the pathogenetically definable events leading to the genesis of breast cancer.