Biomarker Of Oxidative DNA Damage Research Articles

Measurement of uranium concentrations in urine samples of adult healthy groups in Najaf governorate with estimation of urine concentrations of 8-OHdG compound as biomarker for DNA damage

In this study, 88 healthy adults in Al-Najaf governorate of Iraq have been divided into three groups according to the type of exposure to radiation including environmentally uranium exposures n=29 (G1), occupationally exposures n=27 (G2), and non-uranium exposures n=32 (G3). All groups were subjected for estimation of uranium concentration in urine samples using CR-39 SSNTD method beside measurement of urine concentrations of 8-OHdG compound as a biomarker for oxidative DNA damage using Elisa technique. Reactive oxygen species produced under the effect of many causes including ionizing radiation exposure, (0 H)free radical induced the formation of 8-OHdG compound from cellular and mitochondrial DNA through attack of C-8 in purine ring of guanine base. The results showed that mean values of uranium concentration were (1.836±0.426 μg/L), (2.02±0.404 μg/L) and (1.755± 0.437 μg/L) for group1, group2 and group3, respectively. While mean values for 8-OHdG were (49.810±15.484 ng/ml), (47.717±14.232ng/ml) and (46.769±14.249ng/ml) for the three groups, respectively. No significant statistical differences were recorded between all data obtained. These results suggested the presence of uranium pollution in all groups including the non-exposed group as compared with reference value of (WHO, 2004). Results also demonstrate the presence of DNA oxidative damage in all groups according to concentration levels of 8-OHdG in urine samples. Therefore, the uranium pollution in urine samples of the examined groups indicate the presence of chronic low dose radiation source in Najaf governorate, which might be the cause of DNA damage as reflected by the urinary levels of 8-OHdG compound.

Effects of E-Cigarette Aerosols with Varying Levels of Nicotine on Biomarkers of Oxidative Stress and Inflammation in Mice.

To provide insights into the cause of e-cigarette (e-cig) associated lung injury, we examined the effects of propylene glycol (PG) and glycerol (G), two common solvent carriers used to deliver nicotine/flavor, on markers of oxidative stress and inflammation in female B6C3F1 mice which had been used successfully in tobacco smoke (TS)-induced lung carcinogenesis. Mice exposed to air and TS were used as negative and positive controls, respectively. Using LC-MS/MS, we showed that PG/G alone, in the absence of nicotine, significantly increased the levels of 8-hydroxy-2'-deoxyguanosine (8-OHdG or its tautomer 8-oxodG), a biomarker of DNA oxidative damage, in lung and plasma of mice; moreover, addition of nicotine (12 and 24 mg/mL) in e-cig liquid appears to suppress the levels of 8-oxodG. Exposure to e-cig aerosols or TS induced nonsignificant increases of plasma C-reactive protein (CRP), a biomarker of inflammation; nonetheless, the levels of fibronectin (FN), a biomarker of tissue injury, were significantly increased by e-cig aerosols or TS. Although preliminary, our data showed that exposure to e-cig aerosols induced a higher score of lung injury than did control air or TS exposure. Our results indicate that the B6C3F1 mouse model may be suitable for an in-depth examination of the impact of e-cig on lung injury associated with oxidative stress and inflammation and this study adds to the growing evidence that the use of e-cig can lead to lung damage.

Effects of in vivo treatment of mice with sulforaphane on repair of DNA pyridyloxylbutylation

The phytochemical sulforaphane (SF) has gained interest for its apparent association with reduced cancer risk and other cytoprotective properties, at least some of which are attributed to activation of the transcription factor Nrf2. Repair of bulky DNA adducts is important for mitigating carcinogenesis from exogenous DNA damaging agents, but it is unknown whether in vivo treatment with SF affects adduct repair. At 12 h following a single oral dose of 100 mg/kg SF, an almost doubling in activity for repair of pyridyloxobutylated DNA was observed in CD-1 mouse liver nuclear extracts, but not in lung extracts. This change at 12 h in repair activity was preceded by the induction of Nrf2-regulated genes but not accompanied by changes in levels of the specific nucleotide excision repair (NER) proteins XPC, XPA, XPB and p53 or in binding of hepatic XPC, XPA and XPB to damaged DNA. SF also did not significantly alter histone deacetylase activity as measured by acetylated histone H3 levels, or stimulate formation of γ-H2A.X, a marker of DNA damage. A significant reduction in oxidative DNA damage, as measured by 8-OHdG (a biomarker of oxidative DNA damage), was observed only in DNA from the lungs of SF-treated mice 3 h post-dosing. These results suggest that the ability of SF to increase bulky adduct repair activity is organ-selective and is consistent with activation of the Nrf2 signaling pathway.

Nanostructured material-based electrochemical sensing of oxidative DNA damage biomarkers 8-oxoguanine and 8-oxodeoxyguanosine: a comprehensive review.

Oxidative DNA damage plays an important role in the pathogenesis of various diseases. Among oxidative DNA lesions, 8-oxoguanine (8-oxoG) and its corresponding nucleotide 8-oxo-2'-deoxyguanosine (8-oxodG), the guanine and deoxyguanosine oxidation products, have gained much attention, being considered biomarkers for oxidative DNA damage. Both 8-oxoG and 8-oxodG are used to predict overall body oxidative stress levels, to estimate the risk, to detect, and to make prognosis related to treatment of cancer, degenerative, and other age-related diseases. The need for rapid, easy, and low-cost detection and quantification of 8-oxoG and 8-oxodG biomarkers of oxidative DNA damage in complex samples, urine, blood, and tissue, caused an increasing interest on electrochemical sensors based on modified electrodes, due to their high sensitivity and selectivity, low-cost, and easy miniaturization and automation. This review aims to provide a comprehensive and exhaustive overview of the fundamental principles concerning the electrochemical determination of thebiomarkers 8-oxoG and 8-oxodG using nanostructured materials (NsM), such as carbon nanotubes, carbon nanofibers, graphene-related materials, gold nanomaterials, metal nanoparticles, polymers, nanocomposites, dendrimers, antibodies and aptamers, and modified electrochemical sensors.

Exposure to volatile organic compounds may be associated with oxidative DNA damage-mediated childhood asthma

Volatile organic compounds (VOCs) are important and ubiquitous air pollutants, which may lead to a significant increase in the prevalence of respiratory diseases. To investigate the relationships between VOCs exposure and childhood asthma, 252 asthmatic children and 69 healthy children were recruited. Urinary 8-hydroxy-2′-deoxyguanosine (8-OHdG, a biomarker of oxidative DNA damage), trans-3′-hydroxycotinine (OH-Cot, a biomarker of passive smoking) and 27 VOC metabolites were simultaneously determined by an ultra-high-performance liquid chromatography-tandem mass spectrometer. Results showed that levels of 8-OHdG and most VOC metabolites in asthmatic children were significantly higher than those in healthy children. More than half of the VOC metabolites were significantly and positively associated with OH-Cot with maximal β coefficient of 0.169, suggesting that second-hand smoking is one important source of VOCs exposure for children in Guangzhou. Significant dose-response relationships between most VOC metabolites and 8-OHdG were observed. Each unit increase in ln-transformed VOC metabolite levels was significantly associated with 5.5–32% increase in ln-transformed 8-OHdG level. Moreover, each unit increase in ln-transformed 8-OHdG level was associated with an 896% increased odd ratios (OR) of asthma in children (OR = 9.96, 95% confidence intervals (CI): 4.75, 20.9), indicating that oxidative stress induced by VOCs exposure may have a significant impact on childhood asthma. Urinary 3-&4-Methylhippuric acid (3-&4-MHA, OR: 5.78, 95% CI: 3.50, 9.54), rac 2-Aminothiazoline-4-carboxylic acid (ATCA, OR: 2.90, 95% CI: 1.69, 4.99) and N-Acetyl-S-(3,4-dihydroxybutyl)-L-cysteine (DHBMA, OR: 2.76, 95% CI: 1.73, 4.43) which may derive from m/p-xylene, cyanide and 1,3-butadiene exposure, respectively, could significantly and maximally increase the odds of asthma. Interestingly, they also had the strongest associations with 8-OHdG among all investigated VOC metabolites. Moreover, DHBMA strongly correlated with most VOC metabolites. Hence, DHBMA is a suitable biomarker to indicate not only VOCs exposure profile, but also the DNA damage-mediated asthma induced by VOCs.

OGG1 DNA Repair Gene Polymorphism As a Biomarker of Oxidative and Genotoxic DNA Damage.

Background:Single nucleotide polymorphisms in OGG1 gene modulates DNA repair capacity and functions as one of the first lines of protective mechanisms against 8-OHdG mutagenicity. OGG1-Cys326 gene polymorphism may decrease DNA repair function, causing oxidative stress due to higher oxidative DNA damage. The main purpose of this study was to examine the link of oxidative and genotoxic DNA damage with DNA repair OGG1 gene polymorphism, in charcoal workers exposed to polyaromatic hydrocarbons. Methods:Urinary 8-OHdG excretion (a biomarker of oxidative DNA damage) was determined in both exposed and control populations. Genotyping of OGG1 DNA repair gene in the blood samples of subjects was carried out by PCR-RFLP method. Results:The 8-OHdG urinary concentration was significantly higher (p < 0.05) in the exposed (geometric mean 12.33 ± 3.78) than in the unexposed (geometric mean 7.36 ± 2.29) population. DNA damage, as measured by 8-OHdG and TM content, was found to be significantly higher in OGG1 homozygous mutants (mt/mt; 18.81 ± 3.34; 6.04 ± 0.52) as compared to wild-type genotypes (wt/wt; 10.34 ± 2.25; 5.19 ± 2.50) and heterozygous (wt/mt) mutants (12.82 ± 2.81; 6.04 ± 0.93) in the exposed group. Conclusion:We found a significant association of OGG1 heterozygous (wt/mt) and homozygous (mt/mt) variants with oxidative and genotoxic damage, suggesting that these polymorphisms may modulate the effects of PAH exposure in occupational workers.

The Effects of Combined Physical Exercise on Serum Redox Biomarkers and Leukocyte DNA Damage of Obese Women.

Obesity is usually linked to oxidative stress, which can lead to damage to biomolecules. The combination of aerobic and strength exercises seems to induce health benefits in obese individuals, but little is known about the effects of combined physical exercise on redox homeostasis and DNA damage in this population. Thus, the aim of the current study was to determine the effects of 16 weeks of combined physical exercise on biomarkers of oxidative stress and DNA damage in obese women. 17 obese women underwent 16 weeks of a combined physical training program, 3 times per week. Anthropometric and biochemical parameters, serum superoxide dismutase (SOD) and glutathione peroxidase activity, plasma 8-isoprostane levels, and DNA and chromosomal damage were evaluated before and after physical training. Combined physical exercise training decreased body weight (83.2 ± 9.6 vs. 80.2 ± 9.6 kg), body mass index (33.8 ± 3.6 vs. 32.6 ± 3.7 kg·m−2), body fat (40.2 ± 2.6 vs. 39.0 ± 3.2%), and waist circumference (99.3 ± 9.4 vs. 94.1 ± 8.8 cm), while the fat-free mass was augmented (59.9 ± 2.9 vs. 60.7 ± 3.1 kg). Moreover, blood glucose reduced (113.5 ± 29.6 vs. 107.3 ± 28.9 mg/dL) along with high-density lipoprotein (54.6 ± 18.1 vs. 59.0 ± 18.8 mg/dL), TSH (2.1 ± 1.1 vs. 2.6 ± 1.2 mIU/mL), and free T4 (0.9 ± 0.1 vs. 1.12 ± 0.2 ng/dL) increase after physical exercise training. Plasma 8-isoprostane levels (17.24 ± 7.9 vs. 29.11 ± 17.44 pg/mL) and DNA damage (34.16 ± 7.1 vs. 45.96 ± 5.8% DNA in tail) were also higher after physical training. No changes were observed in chromosomal damage levels. These results suggest that 16 weeks of combined exercise training 3 times per week is effective in reducing body fat but also increases oxidative stress and DNA damage in obese women.

Histones participate in base excision repair of 8-oxodGuo by transiently cross-linking with active repair intermediates in nucleosome core particles.

8-Oxo-7,8-dihydro-2′-deoxyguanosine (8-oxodGuo) is a biomarker of oxidative DNA damage and can be repaired by hOGG1 and APE1 via the base excision repair (BER) pathway. In this work, we studied coordinated BER of 8-oxodGuo by hOGG1 and APE1 in nucleosome core particles and found that histones transiently formed DNA-protein cross-links (DPCs) with active repair intermediates such as 3′-phospho-α,β-unsaturated aldehyde (PUA) and 5′-deoxyribosephosphate (dRP). The effects of histone participation could be beneficial or deleterious to the BER process, depending on the circumstances. In the absence of APE1, histones enhanced the AP lyase activity of hOGG1 by cross-linking with 3′-PUA. However, the formed histone-PUA DPCs hampered the subsequent repair process. In the presence of APE1, both the AP lyase activity of hOGG1 and the formation of histone-PUA DPCs were suppressed. In this case, histones could catalyse removal of the 5′-dRP by transiently cross-linking with the active intermediate. That is, histones promoted the repair by acting as 5′-dRP lyases. Our findings demonstrate that histones participate in multiple steps of 8-oxodGuo repair in nucleosome core particles, highlighting the diverse roles that histones may play during DNA repair in eukaryotic cells.

Oxidative stress markers in patient-derived non-cancerous cervical tissues and cells

High-risk human papillomaviruses (HPV) are the causative agents of cervical cancer. However, not all infected women develop cervical cancer. Cervical tumorigenesis is characterized by a multifactorial etiology, with oxidative stress (OS) likely playing a major role. In addition to exogenous sources, metabolic processes also contribute to OS. In principle, variability in levels of cervical OS has the potential to influence the likelihood of conversion to cervical cancer. To ask whether such variability indeed existed, we assessed the levels of ROS and the oxidative DNA damage biomarker 8-oxodG in normal non-cancerous cervical tissues and cells obtained from women with uterovaginal pelvic organ prolapse following vaginal hysterectomy. We demonstrated five and ten-fold variability between tissues isolated from the transformation zone (TZ) and ectocervix (EC) of different women, respectively. Despite the greater variability (likely due to differences in tissue composition), the overall pattern of ROS levels in EC tissues mirrored those obtained in their corresponding TZ tissues. Our results also show that the levels of ROS in TZ tissues were always higher than or equal to those found in the respective EC tissues, providing a possible explanation for TZ tissue being the primary target for HPV infection and cervical carcinogenesis. Interestingly, primary keratinocytes isolated and cultured from these cervical specimens also displayed high variability in ROS levels, with some strongly mirroring the levels of ROS observed in their corresponding tissues, while others were less closely associated. Finally, we demonstrated that the levels of DNA damage mirrored the levels of ROS in the cultured primary cells. Understanding the factors and mechanisms that dispose certain individuals to develop cervical cancer has the potential to enable the development of approaches that make the conversion of HPV infection to cancer development even more rare.

The acute response profile of inflammatory and oxidative stress biomarkers in welders

Objectives: Welding fume is an occupational hazard that can cause a variety of health effects. We aimed to investigate inflammatory response profile and oxidative stress level after acute welding fume exposure. Methods: In 87 US adult boilermakers, we took measurements repeatedly immediately before and after a welding shift, as well as at two matched time points on non-welding days, following a self-controlled design. The measured plasma inflammatory biomarkers include IL-1β, IL-2, IL-6, IL-8, IL-10, TNF-α, VEGF, CRP, SAA, sICAM-1, and sVCAM-1; while urinary 8-isoprostane and 8-OHdG were measured as oxidative stress and DNA damage biomarkers, respectively. Individual level PM2.5 exposure were measured during the welding task, as well as non-welding days. Results: The average PM2.5 level was significantly higher during welding shifts, compared to baseline measured on non-welding days (0.42 vs. 0.12 mg/m3, p&lt;0.01). The log(u-8-isoprostane) increased 0.21 unit (p&lt;0.01) after welding shift, but did not change (p=0.91) during the matched period on non-welding days, adjusted for covariates. In a balanced subset, we observed the same but insignificant trend. Log(u-8-OHdG) was 0.07 unit higher (p=0.04) on welding days, at both time points. Also, log(IL-6) had opposite trends between welding shift and self-control (pinteraction=0.03). We found u-8-isoprostane and u-8-OHdG to be higher among smokers, and non-smokers were more sensitive to the effect of welding fume exposure. Conclusions: We studied the controlled health effect of welding fume exposure, and captured indicative signals, but it subjected to insufficient power. The result could promote understanding about pathogenesis of occupational diseases.

Direct and Oxidative DNA Damage in a Group of Painters Exposed to VOCs: Dose - Response Relationship.

Volatile organic compounds (VOCs) are present in several working activities. This work is aimed at comparing oxidative stress and DNA damage biomarkers to specific VOCs in the occupational exposure of painters. Dose-response relationships between biomarkers of oxidative stress and of dose were studied. Unmetabolized VOCs and their urinary metabolites were analyzed. Urinary Methylhyppuric acids (MHIPPs, xylenes metabolite), Phenylglyoxylic and Mandelic acid (PGA, MA ethylbenzene metabolites), S-Benzylmercapturic acid (SBMA, toluene metabolite), and S-Phenylmercapturic acid (SPMA, benzene metabolite) were quantified at the end of work-shift. Oxidative stress was determined by: urinary excretion of 8-oxodGuo, 8-oxoGua and 8-oxoGuo and direct/oxidative DNA damage in blood by Fpg-Comet assay. Multivariate linear regression models were used to assess statistical significance of the association between dose and effect biomarkers. The regressions were studied with and without the effect of hOGG1 and XRCC1 gene polymorphisms. Statistically significant associations were found between MHIPPs and both 8-oxoGuo and oxidative DNA damage effect biomarkers measured with the Comet assay. Oxidative DNA damage results significantly associated with airborne xylenes and toluene, whilst 8-oxodGuo was significantly related to urinary xylenes and toluene. Direct DNA damage was significantly associated to SBMA. XRCC1 wild-type gene polymorphism was significantly associated with lower oxidative and total DNA damage with respect to heterozygous and mutant genotypes. The interpretation of the results requires some caution, as the different VOCs are all simultaneously present in the mixture and correlated among them.

Protamine-2 Deficiency Initiates a Reactive Oxygen Species (ROS)-Mediated Destruction Cascade during Epididymal Sperm Maturation in Mice.

Protamines are the safeguards of the paternal sperm genome. They replace most of the histones during spermiogenesis, resulting in DNA hypercondensation, thereby protecting its genome from environmental noxa. Impaired protamination has been linked to male infertility in mice and humans in many studies. Apart from impaired DNA integrity, protamine-deficient human and murine sperm show multiple secondary effects, including decreased motility and aberrant head morphology. In this study, we use a Protamine-2 (Prm2)-deficient mouse model in combination with label-free quantitative proteomics to decipher the underlying molecular processes of these effects. We show that loss of the sperm’s antioxidant capacity, indicated by downregulation of key proteins like Superoxide dismutase type 1 (SOD1) and Peroxiredoxin 5 (PRDX5), ultimately initiates an oxidative stress-mediated destruction cascade during epididymal sperm maturation. This is confirmed by an increased level of 8-OHdG in epididymal sperm, a biomarker for oxidative stress-mediated DNA damage. Prm2-deficient testicular sperm are not affected and initiate the proper development of blastocyst stage preimplantation embryos in vitro upon intracytoplasmic sperm injection (ICSI) into oocytes. Our results provide new insight into the role of Prm2 and its downstream molecular effects on sperm function and present an important contribution to the investigation of new treatment regimens for infertile men with impaired protamination.

Higher ultra-processed food intake is associated with higher DNA damage in healthy adolescents.

Ultra-processed food is one of the main contributors to energy supply and consumption in food systems worldwide, and evidence of their detrimental health outcomes in humans is emerging. This study aimed to assess ultra-processed food intake and its association with urinary levels of 8-hydroxy-2'-deoxyguanosine (8-OHdG), a biomarker of DNA oxidative damage, in 139 healthy adolescents in Karaj City in Iran. Usual dietary intake was measured using a 168-item validated FFQ. The daily intake of ultra-processed food consumption was determined through the classification of NOVA, and general linear models were used to compare the urinary levels of 8-OHdG/creatinine (ng/mg creatinine) within tertiles of ultra-processed food intake. Adolescents in the higher tertile of ultra-processed food consumption had a significantly higher mean level of urinary 8-OHdG/creatinine in comparison with the lower tertiles in the crude model (Pfor trend: 0·003) and after adjustment for confounding variables, including total energy intake, sex, age, BMI for age Z-score, obesity and physical activity (Pfor trend: 0·004). This association was still significant after adjusting for dietary intake of whole grains, nuts, legumes, the ratio of MUFA:SFA (g/d) and Mediterranean dietary score (Pfor trend: 0·002). More studies are needed to explore the determinants of ultra-processed food supply, demand, consumption and health effects; such studies should be applied to develop evidence-informed policies and regulatory mechanisms to improve children's and adolescents' food environment policymaking and legislation with special attention to ultra-processed food.

Two Faces of Vitamin C-Antioxidative and Pro-Oxidative Agent.

Vitamin C has been known for decades. It is common in everyday use as an element of the diet, supplementation, and a preservative. For years, research has been conducted to precisely determine the mechanism of action of ascorbate in the cell. Available results indicate its multi-directional cellular effects. Vitamin C, which belongs to antioxidants scavenging free radicals, also has a ‘second face’—as a pro-oxidative factor. However, whether is the latter nature a defect harmful to the cell, or whether a virtue that is a source of benefit? In this review, we discuss the effects of vitamin C treatment in cancer prevention and the role of ascorbate in maintaining redox balance in the central nervous system (CNS). Finally, we discuss the effect of vitamin C supplementation on biomarkers of oxidative DNA damage and review the evidence that vitamin C has radioprotective properties.

Acrylamide Exposure and Oxidative DNA Damage, Lipid Peroxidation, and Fasting Plasma Glucose Alteration: Association and Mediation Analyses in Chinese Urban Adults.

Acrylamide exposure from daily-consumed food has raised global concern. We aimed to assess the exposure-response relationships of internal acrylamide exposure with oxidative DNA damage, lipid peroxidation, and fasting plasma glucose (FPG) alteration and investigate the mediating role of oxidative DNA damage and lipid peroxidation in the association of internal acrylamide exposure with FPG. FPG and urinary biomarkers of oxidative DNA damage (8-hydroxy-deoxyguanosine [8-OHdG]), lipid peroxidation (8-iso-prostaglandin-F2α [8-iso-PGF2α]), and acrylamide exposure (N-acetyl-S-[2-carbamoylethyl]-l-cysteine [AAMA], N-acetyl-S-[2-carbamoyl-2-hydroxyethyl]-l-cysteine [GAMA]) were measured for 3,270 general adults from the Wuhan-Zhuhai cohort. The associations of urinary acrylamide metabolites with 8-OHdG, 8-iso-PGF2α, and FPG were assessed by linear mixed models. The mediating roles of 8-OHdG and 8-iso-PGF2α were evaluated by mediation analysis. We found significant linear positive dose-response relationships of urinary acrylamide metabolites with 8-OHdG, 8-iso-PGF2α, and FPG (except GAMA with FPG) and 8-iso-PGF2α with FPG. Each 1-unit increase in log-transformed level of AAMA, AAMA + GAMA (ΣUAAM), or 8-iso-PGF2α was associated with a 0.17, 0.15, or 0.23 mmol/L increase in FPG, respectively (P and/or P trend < 0.05). Each 1% increase in AAMA, GAMA, or ΣUAAM was associated with a 0.19%, 0.27%, or 0.22% increase in 8-OHdG, respectively, and a 0.40%, 0.48%, or 0.44% increase in 8-iso-PGF2α, respectively (P and P trend < 0.05). Increased 8-iso-PGF2α rather than 8-OHdG significantly mediated 64.29% and 76.92% of the AAMA- and ΣUAAM-associated FPG increases, respectively. Exposure of the general adult population to acrylamide was associated with FPG elevation, oxidative DNA damage, and lipid peroxidation, which in turn partly mediated acrylamide-associated FPG elevation.

Chromatographic Detection of 8-Hydroxy-2'-Deoxyguanosine in Leukocytes of Asbestos Exposed Workers for Assessing Past and Recent Carcinogen Exposures.

Asbestos fibers include a group of silicate minerals that occur in the environment and are widely employed in occupational settings. Asbestos exposure has been associated to various chronic diseases; such as pulmonary fibrosis; mesothelioma; and lung cancer; often characterized by a long period of latency. Underlying mechanisms that are behind the carcinogenic effect of asbestos have not been fully clarified. Therefore; we have conducted an epidemiological study to evaluate the relationship between 8-hydroxy-2′-deoxyguanosine (8-oxodG), one of the most reliable biomarkers of oxidative stress and oxidative DNA damage; and asbestos exposure in the peripheral blood of residents in Tuscany and Liguria regions; Italy; stratified by occupational exposure to this carcinogen. Levels of 8-oxodG were expressed such as relative adduct labeling (RAL); the frequency of 8-oxodG per 105 deoxyguanosine was significantly higher among exposed workers with respect to the controls; i.e., 3.0 ± 0.2 Standard Error (SE) in asbestos workers versus a value of 1.3 ± 0.1 (SE) in unexposed controls (p < 0.001). When the relationship with occupational history was investigated; significant higher levels of 8-oxodG were measured in current and former asbestos workers vs. healthy controls; 3.1 ± 0.3 (SE) and 2.9 ± 0.2 (SE), respectively. After stratification for occupational history; a significant 194% excess of adducts was found in workers with 10 or more years of past asbestos exposure (p < 0.001). 8-oxodG can be used for medical surveillance programs of cohorts of workers with past and recent exposures to carcinogens for the identification of subjects requiring a more intense clinical surveillance.

Oxidative stress, DNA damage and apoptosis levels in those who use borderline high level fluoride content drinking water

Aim: Fluoride is necessary for tooth and bone development, but when exposed to excessive levels can cause oxidative stress, DNA damage, apoptosis, fluorosis and cancer. The aim of this study is to reveal the underlying mechanism of fluoride toxicity and to clarify, in part, the uncertainty of the fluoride level in the reference value ranges of drinking water. Material and Methods: Two groups were included in the study as exposure and control groups. Serum Total Oxidant Status and Total Antioxidant Status were measured with colorimetric; Urine 8-OHdG (8-hydroxy-2-deoxyguanosine) (CUSABIO) levels as DNA damage biomarkers and serum M30 and M65 levels (PEVIVA) as apoptosis biomarkers were studied by ELISA method. In addition, all participants underwent a dental examination by the dentist. Results: Serum total antioxidant status (TAS) were lower in the exposure group compared to the control group (p &amp;lt;0.001); serum total oxidant status (TOS) (p &amp;lt;0.001), OSI (p &amp;lt;0.001), M30 (p &amp;lt;0.001) and M65 (p &amp;lt;0.001) levels and urine 8-OHdG (p = 0.011) levels were high. However, the M30 / M60 ratio was not statistically different between the two groups (p = 0.371). Dental fluorosis was detected in all participants in the exposure group. Conclusion: This study showed increased levels of oxidative stress, DNA damage and apoptosis biomarkers in drinking water users with borderline high level fluoride. Therefore, instead of the World Health Organization's reference value range (0.5-1.5 mg/L) for fluoride levels in drinking water, the US Public Health Service’s (0.7 mg/L) reference value range seems to be more appropriate to the precaution.

Sonochemical preparation of carbon nanosheets supporting cuprous oxide architecture for high-performance and non-enzymatic electrochemical sensor in biological samples.

Copper (Cu) based metal oxides have high electrocatalytic ability. In this work, we are synthesized stone-like cuprous oxide particles (Cu2O SNPs) covered on acid functionalized graphene oxide (GOS) sheets using ultrasonic process (50kHz and 100W). Besides, the chemical structural and crystalline analyses of Cu2O SNPs@GOS composites were characterized by transmission electron microscopy, X-ray crystallography and energy-dispersive X-ray spectroscopy. The Cu2O SNPs@GOS nanomaterials were tested towards detection of 8-hydroxydeoxyguanosine (8-OHdG) in biological samples. As expected Cu2O SNPs@GOS catalyst modified electrodes performed an outstanding catalytic ability on 8-hydroxydeoxyguanosine oxidation. 8-OHdG is oxidative stress biomarker. Further, it is noted that the detection performance of Cu2O SNPs@GOS coated electrodes and it's highly enhanced due to the synergistic effect of Cu2O SNPs and GOS. Besides, the modified materials provide more electro-active faces and as well as rapid electron transport pathway and shorten diffusion. Moreover, oxidation of 8-OHdG sensor is exploring a long linear or working range of 0.02-1465µM and high sensitivity (8.75nM). The viability of the Cu2O SNPs@GOS proposed electrochemical methods have tested, to find out 8-OHdG concentrations in biological fluids (blood serum and urine) with a satisfying recovery ranges.

Serum of 8-OHdG as a potential biomarker of oxidative DNA damage in workers exposed to harmful working environments

In the blood serum of 70% individuals exposed to harmful factors of the working environment, a high level of oxidative stress and the DNA damage marker 8-Hydroxy-2’-Deoxyguanosine (8-OHdG) were detected.

Fucoidan Ameliorates Oxidative Stress, Inflammation, DNA Damage, and Hepatorenal Injuries in Diabetic Rats Intoxicated with Aflatoxin B1.

The current study was carried out to evaluate the ameliorative effect of fucoidan against aflatoxicosis-induced hepatorenal toxicity in streptozotocin-induced diabetic rats. Sixty-four Wister albino male rats were randomly assigned into eight groups (8 rats each) that received normal saline, fucoidan (FUC) at 100 mg/kg/day orally for 4 weeks, streptozotocin (STZ) at 50 mg/kg/i.p. single dose, STZ plus FUC, aflatoxin B1 (AFB1) at 50 μg/kg/i.p. after one month of the beginning of the experiment for 2 weeks, AFB1 plus FUC, STZ plus AFB1, or STZ plus AFB1 and FUC. Injection of rats with STZ induced hyperglycemia. Rats with STZ-induced diabetes, with or without AFB1 intoxication, had significantly elevated activities of serum aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase, and levels of serum urea, creatinine, cholesterol, 8-oxo-2′-deoxyguanosine, interleukin-1β, interleukin-6, and tumor necrosis factor-α. In addition, these rats exhibited increased lipid peroxidation and reduced glutathione concentration and activities of superoxide dismutase, catalase, and glutathione peroxidase enzymes in the hepatic and renal tissues. In contrast, administration of FUC to diabetic rats, with or without AFB1 intoxication, ameliorated the altered serum parameters, reduced oxidative stress, DNA damage, and inflammatory biomarkers, and enhanced the antioxidant defense system in the hepatic and renal tissues. These results indicated that FUC ameliorated diabetes and AFB1-induced hepatorenal injuries through alleviating oxidative stress, DNA damage, and inflammation.