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Exposure to metal dust is a significant occupational hazard for foundry workers. This study aimed to investigate exposure to potentially toxic metals and oxidative stress indices and assess the health risk of occupational exposure to metal dust among foundry workers. Environmental and biological exposures to a cocktail of metals were examined by measuring the concentration of Aluminum (Al), Zinc (Zn), Copper (Cu), Cadmium (Cd), Nickel (Ni), and Chromium (Cr) in the air of the workplace, as well as in the blood of the exposed workers. Malondialdehyde (MDA), reduced blood glutathione (GSH) and urinary 8- hydroxydeoxy guanosine (8-OH-dG) were measured as biomarkers of oxidative stress. All air measurements were below the maximum allowable limits (MAL) except for Al and Ni according to American Conference of Industrial Hygienists (ACGIH) and National Institute of Occupational Safety and Health (NIOSH). Here is significantly elevated Blood Al, Zn, Cu, and Pb levels in exposed workers. Moreover, MDA and 8-OHdG levels significantly increased (P<0.0001). In contrast, the mean level of GSH was reduced considerably in exposed workers compared to the control group (P<0.0001). The MDA acts as a marker with the highest Area Under the Curve (AUC), enabling effective differentiation between the exposed and control subjects (AUC = 0.968; Sensitivity = 90%, Specificity =100%; P <0.0001). Workers occupationally exposed to these metals for prolonged periods possessed higher metal levels in their bodies, which is associated with increased oxidative stress, which consequently causes DNA damage. [ABSTRACT FROM AUTHOR]

Aging is a complex process influenced by internal and external factors. Oxidative stress damages DNA, leading to 8-hydroxy-2' deoxyguanosine formation (8-OHdG). Telomere shortening is considered a biomarker of aging and oxidative stress may enhance its attrition. The ability to manage and repair oxidative stress varies among species and life histories. Avian species, such as Psittacidae birds, exhibit exceptional lifespans despite their physiological characteristics that might suggest otherwise. This study investigates 8-OHdG levels in serum samples from long- and short-lived birds of the order Psittaciformes, examining their relationship with telomere length and antioxidant capacity based on lifespan strategies. Among 43 individuals analyzed 26 belonged to the "long-lived species" group and 17 belonged to the "short-lived species" one. Relative telomere length (rTL) was measured in DNA isolated from whole blood by qPCR, and oxidative stress markers, such as Total Antioxidant Capacity (TAC) and 8-OHdG, were determined by spectrophotometry in serum samples. Long-lived birds had longer rTL than short-lived ones [1.308 ± 0.11 vs. 0.565 ± 0.13, (p < 0.001)]. On the contrary, short-lived birds showed more DNA damage than their counterparts [3.847 ± 0.351 vs. 2.012 ± 0.308, respectively, (p < 0.001)]. Old birds had shorter rTL than young ones, for both longevity groups (p < 0.001). Although no correlation was found between 8-OHdG levels and age, nor 8-OHdG and telomere length, long-lived birds exhibited 75.42-unit increased TAC levels when increased 8-OHdG concentrations (p = 0.046). These findings highlight distinct patterns of telomere length and oxidative stress influenced by lifespan strategies among avian longevity groups. [ABSTRACT FROM AUTHOR]

AbstractObjectivesMethodsResultsConclusionThis study, aimed to determine and compare DNA damage in e-cigarette and HTP (IQOS) users by assessing DNA-adducts, which are biomarkers of various DNA alkylation and oxidation.For the evaluation of DNA alkylation, N3-Ethyladenine (N3-EtA) and N3-Methyladenine (N3-MeA) adducts were used. DNA oxidation was assessed using, 8-hydroxy-2’-deoxyguanosine(8-OHdG). The urinary cotinine, N3-MeA, N3-EtA, and 8-OHdG concentrations of the cigarette smokers (n:39), e-cigarette users (n:28), IQOS users (n:20), passive smokers (n:32), and nonsmokers(n:41) who lived Ankara, Turkiye were determined using, liquid chromatography–tandem mass spectrometry (LC–MS/MS).In light of the detected 8-OHdG levels, e-cigarette (3.19 ng/g creatinine) and IQOS (4.38 ng/g creatinine) users had higher oxidative DNA damage than healthy nonsmokers (2.51 ng/g creatinine). Alkylated DNA-adducts were identified in the urine of e-cigarette (N3-MeA: 3.92 ng/g creatinine; N3-EtA: 0.23 ng/g creatinine) and IQOS (N3-MeA: 7.54 ng/g creatinine; N3-EtA: 0.29 ng/g creatinine) users. In the generation of N3-MeA adducts, a significant difference was found between IQOS users and e-cigarette users (p < 0.05). Also, DNA alkylation in flavored e-cigarette users (N3-MeA: 4.51 ng/g creatinine; N3-EtA: 0.27 ng/g creatinine) was higher than in non-flavored e-cigarette users (N3-MeA: 2.27 ng/g creatinine; N3-EtA: 0.06 ng/g creatinine). The highest cotinine levels were found in cigarette smokers (16.1316 ng/g creatinine). No significant difference was found when e-cigarette (1163.02 ng/g creatinine) and IQOS smokers were compared (1088.3 ng/g creatinine).People who use e-cigarettes and IQOS may be at higher risk of genotoxicity than those who do not use and are not exposed to any tobacco products. Furthermore, the usage of flavoring additives in e-cigarettes contributed to additional genotoxic damage risks. [ABSTRACT FROM AUTHOR]

• Repeated measures were performed in chinese adults with low-moderate arsenic levels. • Arsenic was associated with increased levels of 8-isoPGF2α, 8-OHdG, and PCO. • Arsenic was linked to annual increased rates of 8-isoPGF2α, 8-OHdG, and PCO. • Results remain stable in different models, stratification and sensitivity analyses. Arsenic-related oxidative stress and resultant diseases have attracted global concern, while longitudinal studies are scarce. To assess the relationship between arsenic exposure and systemic oxidative damage, we performed two repeated measures among 5236 observations (4067 participants) in the Wuhan-Zhuhai cohort at the baseline and follow-up after 3 years. Urinary total arsenic, biomarkers of DNA oxidative damage (8-hydroxy-2′-deoxyguanosine (8-OHdG)), lipid peroxidation (8-isoprostaglandin F2alpha (8-isoPGF2α)), and protein oxidative damage (protein carbonyls (PCO)) were detected for all observations. Here we used linear mixed models to estimate the cross-sectional and longitudinal associations between arsenic exposure and oxidative damage. Exposure-response curves were constructed by utilizing the generalized additive mixed models with thin plate regressions. After adjusting for potential confounders, arsenic level was significantly and positively related to the levels of global oxidative damage and their annual increased rates in dose-response manners. In cross-sectional analyses, each 1% increase in arsenic level was associated with a 0.406% (95% confidence interval (CI): 0.379% to 0.433%), 0.360% (0.301% to 0.420%), and 0.079% (0.055% to 0.103%) increase in 8-isoPGF2α, 8-OHdG, and PCO, respectively. More importantly, arsenic was further found to be associated with increased annual change rates of 8-isoPGF2α (β: 0.147; 95% CI: 0.130 to 0.164), 8-OHdG (0.155; 0.118 to 0.192), and PCO (0.050; 0.035 to 0.064) in the longitudinal analyses. Our study suggested that arsenic exposure was not only positively related with global oxidative damage to lipid, DNA, and protein in cross-sectional analyses, but also associated with annual increased rates of these biomarkers in dose-dependent manners. [Display omitted] [ABSTRACT FROM AUTHOR]

Oral cancer has a high worldwide incidence and mortality rate showing an upward trend year by year, predominantly occurring in emerging countries. Oral squamous cell carcinoma (OSCC) is one of the main types of oral cancer, accounting for more than 90% of all cases in oral cancer. To evaluate the diagnostic value of 8-hydroxy-2’-deoxyguanosine (8-OHdG), 8-iso-Prostaglandin F2alpha (8-iso-PGF2α) and tumor necrosis factor (TNF)-α as biomarkers in the early carcinogenesis of erosive oral lichen planus (EOLP) by measuring their levels in the blood of patients with EOLP and oral squamous cell carcinoma (OSCC). A total of 69 patients were enrolled in this case-control study [including an OSCC group (n= 23), an EOLP group (n= 23), and an age- and gender-matched healthy control group (n= 23)]. Blood levels of 8-OHdG, 8-iso-PGF2α and TNF-α were measured using enzyme-linked immunosorbent assay (ELISA). Statistical differences in these indicators among the three groups were analyzed. Plasma levels of 8-OHdG and 8-iso-PGF2α in the OSCC group were significantly higher than those in both the EOLP group and the control group (all P< 0.05); no significant statistical difference was found between the EOLP group and the control group. Serum levels of TNF-α in both the OSCC and EOLP groups were elevated compared with the control group, showing significant differences among all three groups (all P< 0.05). Receiver operating characteristic (ROC) curves revealed that plasma 8-OHdG and 8-iso-PGF2α levels and serum TNF-α levels had diagnostic effects on early carcinogenesis in EOLP patients. When these indicators were combined for diagnosis, the diagnostic effect was enhanced, with an area under the ROC curve (AUC) values of 0.819. 8-OHdG, 8-iso-PGF2α and TNF-α may serve as biological indicators for monitoring the early carcinogenesis of EOLP, and the diagnostic effect was augmented when these indicators were combined. [ABSTRACT FROM AUTHOR]

Context Papillary thyroid cancer (PTC) aggressiveness and metastatic potential are closely associated with angioinvasion. Identifying angioinvasion accurately is imperative for treatment planning and prognosis. Objective This study explores serum biomarkers, including 8-hydroxydeoxyguanosine (8-OHdG) and oxidative status markers (total oxidative capacity, total antioxidant capacity [TAC], and sortilin), as potential indicators of angioinvasion in PTC. Design A cross-sectional study involving 50 angioinvasive patients with PTC (study group) and 30 patients with PTC with low-risk features (reference group). Serum levels of biomarkers were analyzed to determine their association with angioinvasion. Setting Patients were recruited from Department of Endocrinology, Diabetology, and Internal Diseases, Medical University of Bialystok, Poland, ensuring representation from a diverse clinical context. Patients or Other Participants Participants included patients with PTC, with 50 in the study group and 30 in the reference group. Selection criteria, matching characteristics, and participant completion rates were duly recorded. Intervention(s) Serum biomarkers were measured to evaluate their association with PTC angioinvasion. Main Outcome Measure(s) Primary outcome measures included serum levels of 8-OHdG, total oxidative capacity, TAC, and sortilin. Results Serum levels of 8-OHdG and sortilin were significantly elevated in angioinvasive PTC, whereas TAC showed a notable decrease (all P <.01). A regression panel combining TAC, 8-OHdG, and sortilin demonstrated a high area under the curve value (0.963) for angioinvasion discernment. Conclusion Measuring TAC, 8-OHdG, and sortilin levels may serve as potential biomarkers for identifying angioinvasion in PTC. The combined assessment of these biomarkers enhances angioinvasion discernment, aiding risk stratification and personalized treatment decisions. Further validation studies are required before integrating these biomarkers into routine clinical practice. The study adheres to the provided structure, providing concise and supported conclusions based on the results. [ABSTRACT FROM AUTHOR]

Objective: Wound healing is characterized by the removal of dead/damaged tissue, the formation of new tissue, and finally, the restoration of the damaged tissue to its original function, starting from the moment of tissue injury. Vanillic acid (VA) is an important component of wheat bran and can heal wounds thanks to its antioxidant potential. This work aimed to investigate the dose-dependent effects of VA (1-2-4-8-16 and 32 µg/ml) in an in vitro way using a wound healing pattern in fibroblast cells. Methods: The MTT test was performed to determine cell viability 48 hours after VA application to the cells in which the wound model was created (except for the control and wound groups). The cells were examined morphologically with an inverted microscope. ELISA and Real-Time PCR analyses were performed to determine changes in oxidative stress parameters and FN1 and COL1α1 gene expressions. Results: The highest percentage closure rate of fibroblast cells in the in vitro wound pattern analysis and the highest percentage of cell viability by MTT analysis were determined in the VA-32 treated group. Morphological images showed that the evaluated gene expressions increased in fibroblast cells in a VA dose-dependent manner. Conclusion: Our findings demonstrated for the first time that VA promotes cell migration and proliferation by regulating oxidative stress and FN1A and COL1α1 genes. The results of this work are thought to pioneer the use of VA in in vivo wound healing studies. [ABSTRACT FROM AUTHOR]

Background Aflatoxin B1 (AFB1) food contamination is a global health hazard that has detrimental effects on both human and animal health. The objective of the current study is to assess the protective impact of carnosic acid against AFB1-induced toxicities in the liver, kidneys, and heart. Methods Forty male Wistar Albino rats (weighting 180 ~ 200 g) were allocated into 5 groups (8 rats each); the 1st group received saline as served as a control, the 2nd group received carnosic acid (CA100) at a dose of 100 mg/kg bw/day by gavage for 14 days, the 3rd group received AFB1 at a dose of 2.5 mg/kg bw, orally twice on days 12 and 14, the 4th group (AFB1-CA50) received AFB1 as in the 3rd group and CA at a dose of 50 mg/kg bw/day, and the 5th group (AFB1-CA100) received AFB1 as in the 3rd group and CA as in the 2nd group. Results CA significantly decreased the liver enzymes (ALT, AST. ALP), renal function products (LDH, BUN, creatinine), and cardiac enzymes (CK and CK-MB) to control levels after the high increment by AFB1 exposure. Moreover, CA significantly decreased the oxidative stress (MDA, NO, 8-OHdG) and increased the antioxidant enzyme activities (CAT, GSH, GSH-Px, and SOD) after severe disruption of oxidant/antioxidant balance by AFB1 exposure. Interestingly, CA significantly decreased the proinflammatory mediators (IL-6, IL-1β, and TNF-α) to the control levels after severe inflammation induced by AFB1 exposure. Conclusions Conclusively, CA had antioxidant, anti-inflammatory, and anti-DNA damage effects against hepatic, renal, and cardiac AFB1-induced toxicities. [ABSTRACT FROM AUTHOR]

Recycling electronic waste (e-waste) poses risks of metal exposure, potentially leading to health impairments. However, no previous study has focused on this issue in Hong Kong. Therefore, from June 2021 to September 2022, this study collected urine samples from 101 e-waste workers and 100 office workers in Hong Kong to compare their urinary levels of metals using ICP-MS. Among the 15 included metals (with detection rates above the 70 % threshold), eight showed significantly higher urinary concentrations (unit: μg/g creatinine) in e-waste workers compared to office workers: Li (25.09 vs. 33.36), Mn (1.78 vs. 4.15), Ni (2.10 vs. 2.77), Cu (5.81 vs. 9.23), Zn (404.35 vs. 431.52), Sr (151.33 vs. 186.26), Tl (0.35 vs. 0.43), and Pb (0.69 vs. 1.16). E-waste workers in Hong Kong generally exhibited lower metal levels than those in developing regions but higher than their counterparts in developed areas. The urine level of 8-hydroxy-2-deoxyguanosine (8-OHdG) was determined by HPLC-MS/MS, and no significant difference was found between the two groups. Multiple linear regression models revealed no significant association between individual metal and urinary 8-OHdG concentrations. However, the metal mixture was identified to marginally elevate the 8-OHdG concentrations (1.12, 95 %CI: 0.04, 2.19) by quantile g‑computation models, with Mn and Cd playing significant roles in such effect. In conclusion, while the metal levels among Hong Kong e-waste workers compared favorably with their counterparts in other regions, their levels were higher than those of local office workers. This underscores the need for policymakers to prioritize attention to this unique industry.

Aging is a complex process influenced by internal and external factors. Oxidative stress damages DNA, leading to 8-hydroxy-2’ deoxyguanosine formation (8-OHdG). Telomere shortening is considered a biomarker of aging and oxidative stress may enhance its attrition. The ability to manage and repair oxidative stress varies among species and life histories. Avian species, such as Psittacidae birds, exhibit exceptional lifespans despite their physiological characteristics that might suggest otherwise. This study investigates 8-OHdG levels in serum samples from long- and short-lived birds of the order Psittaciformes, examining their relationship with telomere length and antioxidant capacity based on lifespan strategies. Among 43 individuals analyzed 26 belonged to the “long-lived species” group and 17 belonged to the “short-lived species” one. Relative telomere length (rTL) was measured in DNA isolated from whole blood by qPCR, and oxidative stress markers, such as Total Antioxidant Capacity (TAC) and 8-OHdG, were determined by spectrophotometry in serum samples. Long-lived birds had longer rTL than short-lived ones [1.308 ± 0.11 vs. 0.565 ± 0.13, (p

Abstract Aims To estimate the effects of the sodium-glucose cotransporter 2 inhibitor (SGLT2i) on proteinuria and oxidative stress expression in type 2 diabetes patients. Materials and methods 68 patients with type 2 diabetes mellitus (T2DM) were divided into three groups according urinary albumin-to-creatinine ratio (UACR), including T2DM with non-albuminuria group (UACR 300 mg/g). They all received SGLT2 inhibitors (SGLT2i) treatment for 12 weeks. The expression of advanced glycation end products (AGEs) in plasma and 8-hydroxy-2-deoxyguanosine (8-OHdG) in urine were measured as indications of oxidative stress. The 24-hour urine samples were collected to measure the concentration of proteinuria and 8-OHdG before and after 12 weeks SGLT2i treatment. Plasma renin activity (PRA), angiotensin II (Ang II) and Aldosterone (ALD) were measured to evaluate renin angiotensin aldosterone system (RASS) levels. Results After 12 weeks SGLT2 inhibitors treatment, the median values of 24-hour proteinuria decreased in macroalbuminuria compared to baseline (970 vs. 821 mg/d, P = 0.006). The median values of AGEs and 8-OHdG decreased in microalbuminuria and macroalbuminuria groups when compared to baseline, AGEs (777 vs. 136 ug/ml, P = 0.003) and (755 vs. 210 ug/ml, P = 0.001), 8-OHdG (8.00 vs. 1.88 ng/ml, P = 0.001) and (11.18 vs. 1.90 ng/ml, P

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This study aims to analyze post-mortem human cardiac specimens, to verify and evaluate the existence or extent of oxidative stress in subjects whose cause of death has been traced to sepsis, through immunohistological oxidative/nitrosative stress markers. Indeed, in the present study, i-NOS, NOX2, and nitrotyrosine markers were higher expressed in the septic death group when compared to the control group, associated with also a significant increase in 8-OHdG, highlighting the pivotal role of oxidative stress in septic etiopathogenesis. In particular, 70% of cardiomyocyte nuclei from septic death specimens showed positivity for 8-OHdG. Furthermore, intense and massive NOX2-positive myocyte immunoreaction was noticed in the septic group, as nitrotyrosine immunostaining intense reaction was found in the cardiac cells. These results demonstrated a correlation between oxidative and nitrosative stress imbalance and the pathophysiology of cardiac dysfunction documented in cases of sepsis. Therefore, subsequent studies will focus on the expression of oxidative stress markers in other organs and tissues, as well as on the involvement of the intracellular pattern of apoptosis, to better clarify the complex pathogenesis of multi-organ failure, leading to support the rationale for including therapies targeting redox abnormalities in the management of septic patients. [ABSTRACT FROM AUTHOR]

Ionizing radiation (IR) severely harms many organs, especially the hematopoietic tissue, mandating the development of protective nutraceuticals. MRN-100, a hydro-ferrate fluid, has been shown to protect γ -radiated fish against hematopoietic tissue damage and lethality. The current study aimed to examine MRN-100's protective effect against irradiated mice and explore the mechanisms underlying its effect. Mice received a single acute, sub-lethal, 5 Gy, whole body dose of X-ray IR. MRN-100 treatment was administered daily for 2-weeks pre-irradiation until 1-week post-irradiation. Spleen and blood were analysed for oxidative stress, hematological, histological and biochemical parameters. Radiation exposure markedly decreased complete blood count (CBC) parameters including hemoglobin, hematocrit, red blood cells, platelets, white blood cells and lymphocytes, and significantly increased neutrophils. In contrast, MRN-100 supplementation to irradiated mice ameliorated all CBC parameters and protected against DNA damage in both splenic cells and serum. It also had an antioxidant effect, increasing the levels of glutathione, superoxide dismutase, catalase and total antioxidant capacity, which were otherwise decreased by irradiation. MRN-100 intake reduced the oxidative stress biomarker levels of nitric oxide, protein carbonyl, malondialdehyde, reactive oxygen species and 8-hydroxydeoxyguanosine, a marker specific to DNA damage. Furthermore, MRN-100 enhanced serum iron and reversed the radiation-induced elevations of liver enzymes. Finally, MRN-100 protected splenic tissue from irradiation as observed by histology. We conclude that MRN-100 consumption may protect against oxidative stress generated by radiation exposure, suggesting that it may be employed as an adjuvant treatment to prevent radiation's severe damage to important organs. [ABSTRACT FROM AUTHOR]

Aims: To estimate the effects of the sodium-glucose cotransporter 2 inhibitor (SGLT2i) on proteinuria and oxidative stress expression in type 2 diabetes patients. Materials and methods: 68 patients with type 2 diabetes mellitus (T2DM) were divided into three groups according urinary albumin-to-creatinine ratio (UACR), including T2DM with non-albuminuria group (UACR < 30 mg/g), T2DM with microalbuminuria group (30 ≤ UACR ≤ 300 mg/g), T2DM with macroalbuminuria group (UACR>300 mg/g). They all received SGLT2 inhibitors (SGLT2i) treatment for 12 weeks. The expression of advanced glycation end products (AGEs) in plasma and 8-hydroxy-2-deoxyguanosine (8-OHdG) in urine were measured as indications of oxidative stress. The 24-hour urine samples were collected to measure the concentration of proteinuria and 8-OHdG before and after 12 weeks SGLT2i treatment. Plasma renin activity (PRA), angiotensin II (Ang II) and Aldosterone (ALD) were measured to evaluate renin angiotensin aldosterone system (RASS) levels. Results: After 12 weeks SGLT2 inhibitors treatment, the median values of 24-hour proteinuria decreased in macroalbuminuria compared to baseline (970 vs. 821 mg/d, P = 0.006). The median values of AGEs and 8-OHdG decreased in microalbuminuria and macroalbuminuria groups when compared to baseline, AGEs (777 vs. 136 ug/ml, P = 0.003) and (755 vs. 210 ug/ml, P = 0.001), 8-OHdG (8.00 vs. 1.88 ng/ml, P = 0.001) and (11.18 vs. 1.90 ng/ml, P < 0.001), respectively. Partial correlations showed that 8-OHdG were relevant to the baseline 24-h proteinuria (r = 0.389, p = 0.001), the reduction of OHdG (Δ8-OHdG) were positively correlated with the decrease of 24-h proteinuria (Δ24-h proteinuria) after 12 weeks of SGLT2i treatment (r = 0.283, P = 0.031). There was no significant correlation between 24-h proteinuria and AGEs in baseline (r = −0.059, p = 0.640) as well as between ΔAGEs and Δ24-h proteinuria (r = 0.022, p = 0.872) after12 weeks of SGLT2i treatment in T2DM patients. Conclusions: SGLT2i may reduce proteinuria in diabetic nephropathy patients, potentially by inhibiting renal oxidative stress, but not through the AGEs pathway and does not induce RAAS activation. Trial registration: This clinical trial was registered on 15/10/2019, in ClinicalTrials.gov, and the registry number is NCT04127084. [ABSTRACT FROM AUTHOR]

Lung cancer (LC) constitutes an important cause of death among patients with Chronic Obstructive Pulmonary Disease (COPD). Both diseases may share pathobiological mechanisms related to oxidative damage and cellular senescence. In this study, the potential value of leucocyte telomere length, a hallmark of aging, and 8-OHdG concentrations, indicative of oxidative DNA damage, as risk biomarkers of LC was evaluated in COPD patients three years prior to LC diagnosis. Relative telomere length measured using qPCR and serum levels of 8-OHdG were determined at the baseline in 99 COPD smokers (33 with LC and 66 age-matched COPD without LC as controls). Of these, 21 COPD with LC and 42 controls had the biomarkers measured 3 years before. Single nucleotide variants (SNVs) in TERT, RTEL, and NAF1 genes were also determined. COPD cases were evaluated, which showed greater telomere length (p < 0.001) and increased serum 8-OHdG levels (p = 0.004) three years prior to LC diagnosis compared to the controls. This relationship was confirmed at the time of LC diagnosis. No significant association was found between the studied SNVs in cases vs. controls. In conclusion, this preliminary study shows that longer leucocyte telomere length and increased 8-OHdG serum levels can be useful as early biomarkers of the risk for future lung cancer development among COPD patients. [ABSTRACT FROM AUTHOR]

Paratuberculosis, created by Mycobacterium avium subspecies paratuberculosis (MAP), manifests as a chronic affliction marked by persistent diarrhoea and granulomatous enteritis, pervasive in both domestic and global wild ruminants. In this investigation, DNA disruption in lesioned tissues of goat as natural infecte with MAP was pathologically assessed. Accordingly, goats manifesting symptoms suggestive to paratuberculosis, including pronounced emaciation and continual episodic diarrhoea, were subjected to an ELISA diagnostic procedure to ascertain the presence of MAP. This diagnostic approach confirmed the presence of the infectious agent in 20 patients. These patients were subsequently euthanized, and tissue samples from intestinal and regional lenf nods. It were subjected to Hematoxylin and Eosin (HE) staining for histopathological investigatıon, Ziehl Neelsen (ZN) staining to identify acid–fast mycobacteria, γ–H2AX to discern disruptions in double stranded DNA, and 8–Ohdg to detect DNA oxidation by immunohistochemical (IHC) method. Gross anatomical observation serous adipose atrophy, augmented dimensions of mesenterial lymphatic nodes, mucosal hypertrophy and non–retractable mucosal undulations. Histological assessment highlighted epithelial cellular degeneration, an abundance of epithelioid macrophages, lymphocytes, plasmocytes, infiltrating in mucosa. Acid–fast entities, discernible through ZN staining, appeared as luminescent red conglomerates in intestinal and mesenterial tissue. The immunohistochemical analyses evinced positive results for both γ–H2AX and 8–Ohdg across all sampled tissues. Intriguingly, this investigation presented the inaugural global evidence of γ–H2AX and 8–Ohdg expression in a natural MAP infection, demonstrating that this pathological agent precipitates DNA degradation and oxidation, thereby augmenting comprehension of the disease’s pathogenesis.

Despite powerful DNA repair systems, oxidative damage/modification to DNA is an inevitable side effect of metabolism, ionizing radiation, lifestyle habits, inflammatory pathologies such as type-2 diabetes or metabolic syndrome, cancer and natural aging.One of the most common oxidative DNA modifications is 8-OHdG (8‑hydroxy-2′-deoxyguanosine), which is the most widely used marker in research and clinical diagnostics. 8-OHdG is easily and specifically detectable in various samples such as urine, plasma, cells and tissues via a large variety of methods like ELISA, HPLC, chromatographic methods, and immunochemistry.Formed by oxidation of guanine and being representative for the degree of DNA damage, 8-OHdG can be also used as biomarker for risk assessment of various cancers as well as degenerative diseases.Here, we present a highly specific, self-developed 8-OHdG antibody in successful comparison to a commercially one, tested in cells (FF95, HCT116, and HT22) and intestinal tissue, focusing on automatized evaluation via fluorescence/confocal microscopy.

Meltem Oktay,1 Mehmet Aso&gbreve;lu,2 Seyhan Taskin,3 Adnan Kirmit4 1Department of Psychiatry, Istanbul Training and Research Hospital, Istanbul, Turkey; 2Department of Psychiatry, Faculty of Medicine, Harran University, Sanliurfa, Turkey; 3Department of Physiology, Faculty of Medicine, Harran University, Sanliurfa, Turkey; 4Department of Biochemistry, Iskenderun State Hospital, Hatay, TürkiyeCorrespondence: Seyhan Taskin, Department of Physiology Harran University Medical Faculty, Osmanbey Campus, Haliliye, Sanliurfa, 63300, Turkey, Tel +90 4143183000, Fax +90 414318 31 92, Email seyhan_taskin@yahoo.comPurpose: Generalized Anxiety Disorder (GAD) is a chronic disease persisting for at least 6 months, characterized by excessive and continuous anxiety, which leads to evident problems and functional disorders. S100B is a glial protein that plays a role in intercellular communication regulating cell growth and differentiation, and intracellular signal transmission. This study aimed to analyze the serum S100B, 8-OHdG, and oxidative stress levels of patients newly diagnosed with GAD who had not started treatment, to better understand the underlying neurobiological basis of the etiology of GAD.Patients and Methods: Forty-four patients diagnosed with GAD according to DSM-5 diagnostic criteria and 44 healthy controls were included in the study. The Beck Anxiety Inventory (BAI) was used to determine the anxiety levels of the GAD patients. The serum S100B, 8-OHdG, total oxidant status (TOS), and total antioxidant status (TAS) levels were measured in the patient and control groups.Results: The 8-OHdG values of the GAD group were determined to be statistically significantly higher than those of the control group (p=0.028). No significant difference was determined between the GAD patients and the control group in respect of the TAS, TOS, and oxidative stress index (OSI) values (p> 0.05). The S100B levels of the GAD group were found to be higher than those of the control group.Conclusion: The results of this study showed that there could be DNA damage because of oxidative stress in GAD patients. There is a need for further studies to confirm the role of S100B protein in GAD etiology and pathogenesis.Keywords: generalized anxiety disorder, oxidative stress, 8-OHdG, DNA damage, S100B

Background: Periodontitis is universally agreed to be an inflammatory disorder which arises as a consequence of periodontal pathogens interacting with the host’s immune response. A significant and crucial element in the onset and advancement of periodontitis is oxidative stress. 8-OHdG is a molecule that’s considered a significant biomarker of oxidative stress. Aim of the study: Analyzing the salivary levels of 8-OHdG in patients with periodontitis/obesity in comparison to healthy controls with analysis of its correlation with various clinical periodontal parameters. Materials and methods: 110 subjects (30 obese, 30 periodontitis, 30 obese periodontitis and 20 healthy subjects) took part in this study. Samples of saliva were acquired from all subjects before clinical examination. Full periodontal examination was conducted for each participant which entailed plaque index PLI, bleeding on probing BOP, probing pocket depth PPD and clinical attachment loss CAL. We assessed obesity utilizing body mass index BMI. Results: It was showed that periodontitis patients and obese patients had significantly elevated concentrations of salivary 8-OHdG when compared with healthy subjects. Also these levels correlated positively with CAL in obese periodontitis patients. Conclusions: This study revealed an association between 8-OHdG and periodontitis which implies that this biomarker serves a vital part in the periodontal disease process. Moreover, this study showed an association between this biomarker and obesity measures, which suggests that periodontitis and obesity are interconnected via oxidative stress.

Disrupted spermatogenesis and testicular injury are among the devastating outcomes of methotrexate. A major contributor to methotrexate-induced testiculopathy is oxidative damage which triggers apoptosis and altered autophagy responses. Eicosapentaenoic acid ethyl ester (EPA-E) is an antihyperlipidemic derivative of omega-3 fatty acids that exhibited affinity to peroxisome proliferator-activated receptor-γ (PPAR-γ) that possesses both antioxidant and autophagy modulating properties. This is an exploratory study aiming at assessing the effectiveness of EPA-E to alleviate testicular damage induced by methotrexate. The specific exploratory hypothesis of this experiment is: EPA-E administration for 1 week to methotrexate-treated rats reduces testicular damage compared to control rats. As a secondary outcome, we were interested in identifying the implicated mechanism that mediates the action of EPA-E. In adult male Wistar rats, testiculopathy was achieved by a single methotrexate injection (20 mg/kg, ip). Rats received vehicle, EPA-E (0.3 g/kg/day, po) alone or with selective PPAR-γ antagonist (bisphenol A diglycidyl ether, BADGE) at 30 mg/kg/day, ip for 1 week. EPA-E recuperated methotrexate-attenuated serum total testosterone while reduced testicular inflammation and oxidative stress, restoring superoxide dismutase (SOD) while reducing malondialdehyde (MDA) and 8–hydroxy–2′-deoxyguanosine (8-OHdG). Methotrexate-induced testicular apoptosis (caspase-3 and p53) was suppressed upon EPA-E treatment. Besides, EPA-E curbed methotrexate-induced abnormal autophagy by downregulating LC3A/B and beclin-1. Interestingly, BADGE-coadministration reversed EPA-E beneficial actions. Collectively, our findings suggest PPAR-γ role in EPA-E-mediated mitigation of methotrexate-evoked testiculopathy via suppression of oxidative stress, apoptosis, as well as abnormal autophagy. Furthermore, EPA-E could be used as a preventive therapy for some testiculopathies mediated by oxidative stress. [ABSTRACT FROM AUTHOR]

Ionizing radiation is strongly linked to direct or indirect DNA damage, as with the production of reactive oxygen species (ROS), which in turn produce DNA damage products, such as 8-hydroxy-2-deoxyguanosine (8-OHdG). In this study, we aimed to investigate the formation of 8-OHdG after irradiation in patients with non-small cell cancer (NSCLC) and its use as a biomarker. Sixteen patients with squamous and thirty-six patients with non-squamous pathology were included. An enzyme-linked-immunosorbent assay (ELISA) was performed before and after radiation. A dose-dependent relationship was confirmed: 8-OHdG plasma concentrations, increased in the total of NSCLC patients and specifically with a linear correlation in non-squamous pathology; in squamous histology, after an initial increase, a significant decrease followed after 20 Gy dose of irradiation. The pretreatment total irradiated tumor volume (cm3) was positively correlated with 8-OHdG levels in patients with squamous histology. When plotting the 8-OHdG plasma concentration at a 10 Gy irradiation dose to the baseline, the AUC was 0.873 (95% CI 0.614–0.984), p < 0.0001, with an associated criterion value of >1378 as a cutoff (sensitivity 72.7%, specificity 100%). When normalizing this ratio to BSA, the associated criterion cutoff value was >708 (sensitivity of 100%, specificity 80%). Lastly, 8-OHdG levels were closely related with the development of radiation-induced toxicities. [ABSTRACT FROM AUTHOR]

Oxidative stress (OS) has been linked to cell damage and chronic disease development; however, the study of psychological factors related with OS has been limited, as has its relationship with biochemical and personal variables. Therefore, the aim of this study was to evaluate the association between a wide variety of personal, psychological, and biochemical factors with OS in a sample of healthy Mexican people. A total of 134 participants, from which 70 (52%) were women, without known chronic conditions were included in the study, and the molecule 8-hydroxy-2′-deoxyguanosine (8-OHdG) was also measured as a marker of OS. We observed in the multivariate analysis of the whole sample that depressive symptoms (measured with CES-D scale) were the only psychological variable significantly associated (positively) with 8-OHdG. In addition, the following sociodemographic variables were associated with 8-OHdG: age, schooling (positively correlated), and the frequency of vitamins/antioxidant consumption (negatively correlated). The biochemical variables of erythrocytes in urine and amylase were positively correlated with 8-OHdG, while glucose was negatively correlated with it. Additional biochemical variables were associated in the multivariate analysis of each sex, including the positive correlation of LDL-cholesterol, LDH enzyme, lymphocytes, and the negative correlation of phosphorus and eosinophils in women's samples, as well as the positive correlation of potassium, uric acid, and leucocytes in urine and the negative correlation of erythrocytes and lipase in the men's samples. In conclusion, depression was the only psychological variable positively correlated with 8-OHdG after adjusting for confounders, and new associations with biochemical variables were found with some differences between sexes. [ABSTRACT FROM AUTHOR]

Testicular torsion causes ischemia and free radical formation by obstructing vascular flow caused by complete or partial rotation of the testis. Myricetin is a plant-derived flavonoid with various biological effects, such as potent anti-oxidation and anti-inflammatory properties. The study aims to evaluate the protective effects of myricetin on the apoptosis of testicular germ cells after experimental testicular torsion. Twenty-four Wistar albino rats were divided into four groups; Control, Sham, Torsion group (720 deg torsion for 2 h), and Myricetin group (torsion model was created, and myricetin injection (1.5 mg/kg) was done during seven days). End of the experiment, testis tissues were removed and fixed in Bouin's solution. Crossman's triple stain was done to determine the histological changes. Also, 8-OHdG and Caspase-3 immunoreactivities were assessed, and TUNEL staining was done. According to the results, we found that 8-OHdG, Caspase-3 immunoreactivity, and TUNEL-positive cells increased, accompanied by several histopathological changes in the torsion group. In contrast, myricetin significantly attenuated testicular injury by reducing apoptosis and DNA damage. These findings suggest that myricetin protects testes against torsion-induced damage in rats, possibly by reducing oxidative stress and inhibiting apoptosis. Our study provides a theoretical basis for further research into maintaining male reproductive health. [ABSTRACT FROM AUTHOR]

Exposure to heavy metals may cause the overproduction of reactive oxygen species, generating oxidative stress and consequently, various harms to human health. The soil surrounding the Ventanas Industrial Complex, in Puchuncaví and Quintero municipal districts on the central Chilean coast, contains heavy metal concentrations (As, Cu, Pb, Zn, among others) that far exceed the maximum permissible levels established by Italian soil standards (used as a reference). This study aimed to investigate the potential association between heavy metal exposure in humans and the levels of oxidative stress biomarkers in inhabitants of these locations. We took blood samples from 140 adults living in sites with high concentrations of heavy metals in the soil and compared them with blood samples from 140 adults living in areas with normal heavy metal concentrations. We assessed lipid peroxidation, damage to genetic material, and Total Antioxidant Capacity in these blood samples. Our results indicate an association between oxidative damage and heavy metal exposure, where the inhabitants living in exposed areas have a higher level of DNA damage compared with those living in control areas. Given that DNA damage is one of the main factors in carcinogenesis, these results are of interest, both for public health and for public policies aimed at limiting human exposure to environmental pollution. [ABSTRACT FROM AUTHOR]

Purpose: 8-Hydroxy-2'-deoxyguanosine (8-OHdG) is a byproduct of DNA oxidation resulting from free radical attacks. Paradoxically, treatment with 8-OHdG accelerates tissue healing. The aim of this study is to quantify the 8-OHdG response after a single session of exercise in both trained and untrained adults. Methods: A systematic review and meta-analysis of exercise intervention studies measuring changes in blood 8-OHdG following resistance exercise and aerobic exercise were conducted. The literature search included Web of Science, PubMed, BASE, and Scopus, with publications up to February 2023 included. Subgroup analysis of training status was also conducted. Results: Sixteen studies involving 431 participants met the eligibility criteria. Resistance exercise showed a medium effect on increasing circulating 8-OHdG levels (SMD = 0.66, p < 0.001), which was similar for both trained and untrained participants. However, studies on aerobic exercise presented mixed results. For trained participants, a small effect of aerobic exercise on increasing circulating 8-OHdG levels was observed (SMD = 0.42; p < 0.001). In contrast, for untrained participants, a large effect of decreasing circulating 8-OHdG levels was observed, mostly after long-duration aerobic exercise (SMD = -1.16; p < 0.05). Similar to resistance exercise, high-intensity aerobic exercise (5-45 min, =≥75% VO2max) significantly increased circulating 8-OHdG levels, primarily in trained participants. Conclusion: Pooled results from the studies confirm an increase in circulating 8-OHdG levels after resistance exercise. However, further studies are needed to fully confirm the circulating 8-OHdG response to aerobic exercise. Increases in 8-OHdG after high-intensity aerobic exercise are observed only in trained individuals, implicating its role in training adaptation. [ABSTRACT FROM AUTHOR]

Growing evidence suggests that abnormalities in mitochondrial DNA (mtDNA) are involved in the pathogenesis of various inflammatory and immuno-mediated diseases. The present study analysed the entire mitochondrial genome by next-generation sequencing (NGS) in 23 patients with psoriatic arthritis (PsA) and 20 healthy controls to identify PsA-related variants. Changes in mtDNA copy number (mtDNAcn) were also evaluated by quantitative polymerase chain reaction (qPCR) and mtDNA oxidative damage was measured using an 8-hydroxy-2'-deoxyguanosine assay. NGS analysis revealed a total of 435 variants including 187 in patients with PsA only and 122 in controls only. Additionally, 126 common variants were found, of which 2 variants differed significantly in their frequencies among patients and controls (P<0.05), and may be associated with susceptibility to PsA. A total of 33 missense variants in mtDNA-encoded genes for complexes I, III, IV and V were identified only in patients with PsA. Of them, 25 variants were predicted to be deleterious by affecting the functions and structures of encoded proteins, and 13 variants were predicted to affect protein's stability. mtDNAcn analysis revealed decreased mtDNA content in patients with PsA compared with controls (P=0.0001) but the decrease in mtDNAcn was not correlated with patients' age or inflammatory biomarkers (P>0.05). Moreover, a higher level of oxidative damage was observed in patients with PsA compared with controls (P=0.03). The results of the present comprehensive analysis of mtDNA in PsA revealed that certain mtDNA variants may be implicated in the predisposition/pathogenesis of PsA, highlighting the importance of NGS in the identification of mtDNA variants in PsA. The current results also demonstrated that decreased mtDNAcn in PsA may be a consequence of increased oxidative stress. These data provide valuable insights into the contribution of mtDNA defects to the pathogenesis of PsA. Additional studies in larger cohorts are needed to elucidate the role of mtDNA defects in PsA. [ABSTRACT FROM AUTHOR]

Abstract Introduction The low blood flow in ischemic stroke reduces oxygen and glucose and induces a series of reactions that produce free radicals. Free radicals can destroy cell membranes (lipid peroxidation) marked by the elevation of malondialdehyde (MDA), and the damage of deoxyribonucleic acid (DNA) showed by the elevation of 8-hydroxy-2’-deoxyguanosine (8-OHdG). This review aimed to assess and conclude the research-based study systematically to analyze the relationship of MDA/8-OHdG and ischemic stroke. Method Cochrane handbook for systematic reviews, the guideline of preferred reporting items for systematic review and meta-analysis (PRISMA), and synthesis without meta-analysis (SWiM) in systematic reviews: reporting guideline was used as guideline in this systematic review. Inclusion criteria in this review were primary studies of every design, articles published in English around January 2000–December 2021, and the study used human as subject. A systematic literature search was applied in 15 electronic medical journals. The authors assessed the study quality and risk of bias of each included study. Results The authors evaluated 374 studies found in literature searching, 30 studies met the criteria for this review, and then underwent the assessment of study quality and risk of bias. Conclusion MDA has the role as oxidative stress biomarker, outcome predictor, mortality predictor, post-stroke cognitive impairment predictor, post-stroke depression predictor, and hand grip strength predictor of ischemic stroke; while 8-OHdG has the role as oxidative stress biomarker, outcome predictor, mortality predictor, post-stroke cognitive impairment predictor, post-stroke depression predictor of ischemic stroke.

Simple Summary: The development of aquaculture has led to an increased attention towards the welfare of farmed fish. Transportation, a routine procedure in this industry, can be stressful for fish due to handling, air exposure, confinement, and reduced oxygen levels. Therefore, it is crucial to gain insights into optimal practices for organizing transportation, ensuring the well-being of these animals and minimizing excessive stress. The objective of this study was to assess the stress response of meagre juveniles during commercial transport from Monfalcone to Stintino (Italy), which lasted 24 h. Welfare evaluation included measuring cortisol levels in muscle and assessing the potential cellular localization of oxidative stress markers in various organs and tissues. Significant increases in cortisol were observed in the fish during transfer from housing to transport tanks and in subsequent samplings at different phases of transport. This finding suggests that either the animals had insufficient time to recover or the transport conditions were suboptimal. However, in terms of oxidative stress, overall immunohistochemical analysis did not reveal variation in marker localization before and after transport, indicating that the stress experienced by the fish during transportation might have been relatively mild. In aquaculture, the transportation of live fish is a crucial but stress-inducing practice, necessitating a thorough understanding of its impact on fish welfare. This study aimed to assess the physiological stress response of meagre (Argyrosomus regius) juveniles during a 24 h commercial transport by quantifying muscle cortisol levels using a specific radioimmunoassay. Additionally, an immunohistochemical approach was used to detect and localize the cellular distribution of oxidative-stress-related biomarkers within various tissues and organs. The results demonstrated a significant increase in muscle cortisol levels following the loading procedure, remaining elevated above basal levels throughout the 24 h transport period. This effect may be attributed to either insufficient time for recovery from the loading stress or prolonged transportation-related stress. Immunostaining for all the antibodies we examined was observed in multiple tissues and organs, but we found no notable variations among the various transport phases. In conclusion, the observed stress response appears to be mainly linked to loading stress and the transport process itself, emphasizing the importance of implementing appropriate operational procedures to safeguard fish well-being during transport. Nonetheless, the unaltered distribution of oxidative stress markers between the control and transported groups suggests that the experienced stress might be within tolerable limits. [ABSTRACT FROM AUTHOR]

Introduction: Annually, the Malaysian Fire & Rescue Department receive at least 1,500 calls relating to open-burning particularly during the El Niño season. Combatting peatland fire is a lengthy process involving a large participation of the fire squad. Consequently, exposure to cancerous chemicals, specifically dioxins, to the fire-fighters is very high. This study examines the level of 17 congeners of dioxin/furan and its correlation with the level of oxidative stress biomarkers, 8-OHdG in the blood serum of the fire-fighters. Methods: Forty-two fire-fighters from five states in Malaysia identified as having involved with peatland fire extinguishing consented to donate 10 mL of their whole blood taken from cubital fossa. The blood samples were spun at 2,500G for 15 minutes and the separated serum were extracted using Accelerated Solvent Extraction method for analysis of 17 dioxin/furan congeners. A 20µL serum from each sample was drawn for oxidative stress biomarker analysis using enzyme-linked immunosorbent assay (ELISA) and its association with dioxins level. Results: The concentrations of dioxin/furan range between 0.0452 pg/g serum lipid to 1147.41 pg/g serum lipid. The geometric mean concentration of the most toxic congeners, 2,3,7,8-TCDD is 0.065 pg TEQ g-1 serum lipid whereas the mean±SD Control and Expose group are 7.41±5.62 and 15.14±37.06 pg TEQ g-1 serum lipid, respectively. Significantly important, the median (iqr) of the 8-OHdG concentration level detected is 13.00 (20.62) ng/mL ranging between 3.83 ng/mL to 101.00 ng/mL. Conclusion: The study establishes that fire-fighters extinguishing peatland fires are potentially exposed to dioxin/furan that induced the 8-OHdG level. [ABSTRACT FROM AUTHOR]

Cyclophosphamide (CP) is used alone or in combination with other therapeutic agents to treat different malignant tumors. Nephrotoxicity is one of the major side effects of it. Ellagic acid (EA) is a polyphenol, known for its antioxidant properties. In this study, the protective effect of EA on CP-induced renal damage was evaluated. For this purpose, 24 rats were divided into four groups, control, CP, CP+EA50, and CP+EA75. Histopathological examination of kidneys revealed hyperemia, epithelial degeneration, swelling, cystic dilatation and luminal proteinaceous material in tubuli, congested and hypercellular glomeruli and also inflammatory cells infiltration in the cortical and medullary area in CP group. Significant decrease of pathological lesions was found in CP+EA groups especially in the CP+EA75 group. In immunohistochemical sections, 8-hydroxy-2-deoxyguanosine (8-OHdG) and hypoxia-inducible factor-1 alpha (HIF-1α) revealed less positivity in EA received groups but B-cell lymphoma-2 (Bcl-2) revealed more positivity as compared to CP. Both histopathological and immunohistochemical findings revealed that EA has a protective effect against CP-induced renal damage in rats. [ABSTRACT FROM AUTHOR]

Simple Summary: Although oxidative stress regulates essential signaling pathways, oxidative DNA damage causes cancer initiation and progression. Given that the relationship between oxidative stress and colorectal cancer (CRC) remains poorly understood, we performed immunohistochemistry to detect 8-hydroxy-2′ deoxyguanosine (8-OHdG) in 564 patients with CRC and conducted survival analysis based on the pathological stage to identify novel biomarkers. We found that low 8-OHdG levels were associated with a poor prognosis. Further, when 8-OHdG expression was combined with the tumor node metastasis stage, if 8-OHdG expression was low in the same stage, the prognosis was poor, suggesting that 8-OHdG may be an essential biomarker of CRC. The incidence of colorectal cancer (CRC) is increasing worldwide. 8-hydroxy-2′-deoxyguanosine (8-OHdG), one of the most prevalent DNA alterations, is known to be upregulated in several carcinomas; however, 8-OHdG has not been used to predict the prognosis of patients with CRC. We aimed to determine 8-OHdG levels in patients with CRC using immunohistochemistry and conducted a survival analysis according to the pathological stage. The 5-year event-free survival (EFS) and disease-specific survival (DSS) hazard ratios (HRs) of the low 8-OHdG subgroup were 1.41 (95% confidence interval (CI): 1.01–1.98, p = 0.04) and 1.60 (95% CI: 1.12–2.28, p = 0.01), respectively. When tumor node metastasis (TNM) staging and 8-OHdG expression were combined, the 5-year EFS and DSS HRs of patients with CRC with low 8-OHdG expression cancer at the same TNM stage (stage Ⅲ/Ⅳ) were 1.51 (95% CI: 1.02–2.22, p = 0.04) and 1.64 (95% CI: 1.09–2.48, p = 0.02), respectively, compared to those with high 8-OHdG expression cancer, indicating a poor prognosis. Therefore, low 8-OHdG expression is a significant predictive factor for 5-year EFS and DSS in patients with CRC, and it can serve as an essential biomarker of CRC. [ABSTRACT FROM AUTHOR]

Background: Pneumonia causes the majority of acute respiratory distress syndrome (ARDS) cases. The microbes that cause pneumonia are very diverse. In addition to DNA, RNA viruses, Gram-negative and Gram-positive bacteria cause two types of cytokine imbalances, anti-inflammatory and pro-inflammatory. It can also influence the prognosis of sepsis and other infectious diseases. This study aims to search for 8-hydroxy-2'-deoxyguanosine (8-OHdG), IL- 21, IL-23, and c-reactive protein (CRP) and compare cytokine levels. It is also to determine if Pediatric pneumonia patients CRP and cytokine levels correlate with results. Materials and Methods: In the study, blood was drawn from approximately 43 pediatric pneumonia patients and 43 healthy controls who came to the pediatric clinic to investigate serum IL-21, IL-23, 8-OHdG, and CRP levels. The levels of biomarkers were determined by ELISA method. Serum CRP levels were measured using the ATELLICA IM Analyzer. Results: Serum CRP, 8-OHdG, IL-21 and IL-23 levels were significantly higher in the pediatric pneumonia patient group than in the control group. Conclusions: Increased serum IL-21, IL-23, 8-OHdG and CRP expression in pediatric pneumonia patients is a potential determinant suggesting that IL-21, IL-23-related cytokines may play a role in endothelial cell activation reported in patients. Increased 8-OHdG oxidative stress is more pronounced in patients without pediatric pneumonia while pro inflammatory cytokines are higher in pediatric pneumonia patients. However, it is used as a possible therapeutic target to reduce inflammation. Further study on the impact of these findings on comorbidities with larger number test size is needed [ABSTRACT FROM AUTHOR]

The use of nanoparticles like graphene oxide (GO) in nanocomposite industries is growing very fast. There is a strong concern that GO can enter the environment and become nanopollutatnt. Environmental pollutants' exposure usually relates to low concentrations but may last for a long time and impact following generations. Attention should be paid to the effects of nanoparticles, especially on the DNA stability passed on to the offspring. We investigated the multigenerational effects on two strains (wild and long-lived) of house cricket intoxicated with low GO concentrations over five generations, followed by one recovery generation. Our investigation focused on oxidative stress parameters, specifically AP sites (apurinic/apyrimidinic sites) and 8-OHdG (8-hydroxy-2′-deoxyguanosine), and examined the global DNA methylation pattern. Five intoxicated generations were able to overcome the oxidative stress, showing that relatively low doses of GO have a moderate effect on the house cricket (8-OHdG and AP sites). The last recovery generation that experienced a transition from contaminated to uncontaminated food presented greater DNA damage. The pattern of DNA methylation was comparable in every generation, suggesting that other epigenetic mechanisms might be involved. [ABSTRACT FROM AUTHOR]

Objectives: To explore the impact of modernization on oxidative stress during a momentous health transition process, we investigated differences in oxidative stress among the indigenous populations of villages in northern Laos with different levels of modernization. Methods: We conducted a cross‐sectional study of 380 adults in three villages with different levels of modernization. Three biomarkers related to oxidative stress were measured: urinary 8‐hydroxy‐2′‐deoxyguanosine (8‐OHdG) and 8‐isoprostane concentrations (both measured by liquid chromatography–tandem mass spectrometry), and blood telomere length (measured with qPCR). We examined associations between village‐level modernization and oxidative stress‐related biomarkers in a multilevel analysis including a random effect and covariates. Results: The geometric means of urinary 8‐OHdG and 8‐isoprostane concentrations were 2.92 and 0.700 μg/g creatinine, respectively, in our study population. Higher urinary 8‐OHdG concentrations and shorter telomeres were observed in participants from the more modernized villages, whereas urinary 8‐isoprostane concentrations did not differ significantly among villages. Conclusions: Our findings imply that modernization‐induced changes in lifestyle may increase oxidative DNA damage. Baseline levels of oxidative lipid damage are expected to be high in the indigenous populations of northern Laos. Assessments of oxidative stress may provide valuable insights into the mechanisms of health transition in specific populations. [ABSTRACT FROM AUTHOR]

Radiotherapy, which is routinely used to treat a wide range of oncological disorders, primarily affects the malignant tissue in the targeted area, but also have negative effects in the surrounding tissues. Pelvic radiotherapy causes early and late effects on the colon and rectum. Resveratrol (RVT) has been revealed to have a number of pharmacological effects in a variety of experimental models and clinical circumstances, therefore it has piqued the interest of scientists in recent years. In this study, we aimed to investigate the potential protective effects of resveratrol (RVT), a strong antioxidant, anti-inflammatory and anti-mutagenic agent, against toxicity of colonic and rectal tissues seen in the early and late stages after pelvic radiation. The treatment durations of the current study were designed as one week and ten weeks interval by following radiation exposure. Sprague Dawley rats were divided into 5 groups (8 animals/group) as the control, radiation-early effects (Rd-E), radiation-late effects (Rd-L), and RVT-treated Rd-E (Rd-E+RVT) and RVT-treated Rd-L (Rd-L+RVT) groups. İonizing radiation was performed to the pelvic area that covers colon and rectum in single fraction of 20 Gy in a linear accelerator using with 6 MV photon energy. RVT was orally administered (10 mg/kg/day) immediately following the radiation exposure and continued daily for 1 and 10 weeks for early and late groups, respectively. Pelvic radiation caused a significant decrease in glutathione level, while malondialdehyde levels, myeloperoxidase activity and 8-hydroxydeoxyguanosine were increased in both Rd-E and Rd-L groups in the colon and rectum tissues. Additionally, light microscopic evaluations (H&E staining) revealed degeneration of epithelium and inflammatory cell infiltration in the colonic and rectal tissues in radiation groups. RVT treatment reversed all conducted biochemical parameters and ameliorated histomorphological changes following early and late effects of pelvic radiation in tissues. In conclusion, resveratrol may be a candidate as a radioprotector for normal tissues during and after radiotherapy. [ABSTRACT FROM AUTHOR]

Introduction: The low blood flow in ischemic stroke reduces oxygen and glucose and induces a series of reactions that produce free radicals. Free radicals can destroy cell membranes (lipid peroxidation) marked by the elevation of malondialdehyde (MDA), and the damage of deoxyribonucleic acid (DNA) showed by the elevation of 8-hydroxy-2'-deoxyguanosine (8-OHdG). This review aimed to assess and conclude the research-based study systematically to analyze the relationship of MDA/8-OHdG and ischemic stroke. Method: Cochrane handbook for systematic reviews, the guideline of preferred reporting items for systematic review and meta-analysis (PRISMA), and synthesis without meta-analysis (SWiM) in systematic reviews: reporting guideline was used as guideline in this systematic review. Inclusion criteria in this review were primary studies of every design, articles published in English around January 2000–December 2021, and the study used human as subject. A systematic literature search was applied in 15 electronic medical journals. The authors assessed the study quality and risk of bias of each included study. Results: The authors evaluated 374 studies found in literature searching, 30 studies met the criteria for this review, and then underwent the assessment of study quality and risk of bias. Conclusion: MDA has the role as oxidative stress biomarker, outcome predictor, mortality predictor, post-stroke cognitive impairment predictor, post-stroke depression predictor, and hand grip strength predictor of ischemic stroke; while 8-OHdG has the role as oxidative stress biomarker, outcome predictor, mortality predictor, post-stroke cognitive impairment predictor, post-stroke depression predictor of ischemic stroke. [ABSTRACT FROM AUTHOR]

Objectives: Oxidative stress is associated with the development and progression of chronic kidney disease (CKD) in humans. The aim of this study was to evaluate the concentrations of oxidative stress markers, 8-hydroxy-2′-deoxyguanosine (8-OHdG) and malondialdehyde (MDA), in the plasma and urine of cats with different stages of CKD. Methods: Plasma and urine samples were collected from cats with CKD that were referred to the Veterinary Medical Center of the University of Tokyo between April 2019 and October 2022. Plasma and urine samples were collected from healthy cats (n = 6 at most), cats with stage 2 CKD (n = 8) and stage 3–4 CKD (n = 12), and cats with idiopathic cystitis (disease control, n = 5). Plasma and urine concentrations of 8-OHdG and MDA were measured using ELISA and thiobarbituric acid reactive substances assay kits, respectively. Results: The median plasma 8-OHdG concentrations were 0.156 ng/ml (<0.125–0.210 ng/ml) in the healthy group, <0.125 ng/ml (range <0.125 ng/ml) in the idiopathic cystitis group, 0.246 ng/ml (range 0.170–0.403 ng/ml) in cats with stage 2 CKD and 0.433 ng/ml (range 0.209–1.052 ng/ml) in cats with stage 3–4 CKD. Concentrations in stage 3–4 CKD were significantly higher than those in the healthy and disease control groups. Plasma MDA concentrations were low in the healthy and disease control groups and significantly higher in cats with stage 3–4 CKD. In every cat with CKD, plasma 8-OHdG and MDA concentrations were positively correlated with plasma creatinine concentrations (8-OHdG, r s = 0.68; MDA, r s = 0.67). Urinary 8-OHdG/urinary creatinine (u-CRE) and urinary MDA/u-CRE levels did not differ significantly between the groups; however, it was difficult to evaluate them because of the small sample size. Conclusions and relevance: This report shows that plasma 8-OHdG and MDA concentrations increase with the severity of feline CKD. These markers may be useful for assessing oxidative stress in cats with CKD. [ABSTRACT FROM AUTHOR]

Background/Purpose: This research was performed to determine the effect of naringenin (NAR) in experimental hyperuricemia (HU) induced by potassium oxonate (PO) on uric acid levels and xanthine oxidase (XO), inflammation, apoptotic pathway, DNA damage, and antioxidant system in kidney tissue. Study Design: Wistar Albino rats were categorized into four groups: (1) Control group, (2) PO group, (3) [PO+NAR] (2 weeks) group, and (4) PO (2 weeks)+NAR (2 weeks) group. Methods: The first group was not administered any drug. In group 2, PO was administered intraperitoneally 250 mg/kg/day for 2 weeks. In the third group, 100 mg/kg/day NAR was given intraperitoneally 1 hr after PO injection for 2 weeks. In the fourth group, PO was injected for the first 2 weeks, followed by NAR injection for the second 2 weeks. Serum uric acid levels, XO, nuclear factor-kappa B, tumor necrosis factor-alpha, interleukin-17, cytochrome c, 8-Hydroxydeoxyguanosine (8-OHdG), glutathione peroxidase (GPx), and caspase-3 levels in kidney were determined. Results: HU increased the levels of inflammatory and apoptotic parameters, XO, and 8-OHdG levels in kidney. Administration of NAR caused a decrease in these values and an increase in GPx levels. Conclusions: The results of the study show that NAR treatment reduces serum uric acid levels, and apoptosis, inflammation, and DNA damage; increases antioxidant activity in kidney in experimental HU. [ABSTRACT FROM AUTHOR]

Objectives To investigate the association between oxidative stress and erectile dysfunction (ED) in community-dwelling men and men on dialysis.Methods This cross-sectional study included 398 community-dwelling men and 42 men on dialysis. Oxidative stress was assessed using 8-hydroxy-2'-deoxyguanosine (8-OHdG). Univariable and multivariable logistic regression analyses were performed to evaluate the association between oxidative stress and ED.Results Spearman’s rank correlation test showed no significant correlation between urine 8-OHdG levels and the 5-Item International Index of Erectile Function scores in community-dwelling men (ρ = −0.005, p = 0.917) and between plasma 8-OHdG levels and the Sexual Health Inventory for Men scores in men on dialysis (ρ = 0.166, p = 0.295). In community-dwelling men, univariable and multivariable analyses revealed that urine 8-OHdG level was not significantly associated with ED (odds ratio [OR]: 1.005, 95% confidence interval [CI]: 0.884–1.144, p = 0.934; OR: 0.930, 95% CI: 0.798–1.084, p = 0.353; respectively). In men on dialysis, univariable analyses revealed that plasma 8-OHdG level was not significantly associated with severe ED (OR: 0.967, 95% CI: 0.876–1.066, p = 0.498).Conclusions Oxidative stress was not significantly associated with ED prevalence and severity in community-dwelling men and men on dialysis.

Oral GSH supplementation along with antidiabetic treatment was shown to restore the body stores of GSH significantly and reduce oxidative DNA damage (8-OHdG) in Indian Type 2 diabetic (T2D) patients over 6 months in our recent clinical study. Post hoc analysis of the data also suggested that elder patients benefit from improved HbA1c and fasting insulin. We modeled longitudinal changes in diabetic individuals using a linear mixed-effects (LME) framework and obtained i) the distribution of individual trajectories with and without GSH supplementation and ii) the overall rates of changes in the different study arms. Serial changes in elder and younger diabetic individuals were also modeled independently to examine differences in their progression. The average linear trajectories obtained from the model explain how biochemical parameters in T2D patients progress over 6 months on GSH supplementation. Model estimates show improvements in erythrocytic GSH of 108 µM per month and a reduction in 8- OHdG at a rate of 18.5 ng/μg DNA per month in T2D patients. GSH replenishes faster in younger people than in the elder. 8-OHdG reduced more rapidly in the elder (24 ng/μg DNA per month) than in younger (12 ng/μg DNA per month) individuals. Interestingly, elder individuals show a substantial reduction in HbA1c (0.1% per month) and increased fasting insulin (0.6 µU/mL per month). Changes in GSH correlate strongly with changes in HbA1c, 8-OHdG, and fasting insulin in the elder cohort. The model estimates strongly suggest it improves the rate of replenishment in erythrocytic GSH stores and reduces oxidative DNA damage. Elder and younger T2D patients respond differently to GSH supplementation: It improves the rate of reduction in HbA1c and increases fasting insulin in elder patients. These model forecasts have clinical implications that aid in personalizing treatment targets for using oral GSH as adjuvant therapy in diabetes. [ABSTRACT FROM AUTHOR]

Background: The identification of genoprotectants is a promising strategy for improving human health. Piper longum has drawn scientific attention because of its diverse biological effects and traditional utilization. The current investigation aims to evaluate the genome-stabilizing potential of Piper longum against cyclophosphamide-associated genotoxicity. Methods: We adopted a funnel screening with a three-tier evaluation approach, where Piper longum was investigated in an acellular medium, peripheral blood lymphocytes, and a rodent model. The genoprotective action of the Piper longum extract was initially performed with plasmid pBluescript SK(-) DNA. Furthermore, the extract and various fractions were screened against cyclophosphamideinduced genotoxicity using a cytokinesis-block micronucleus assay and a chromosomal aberration assay in human peripheral blood lymphocytes. The genome-stabilizing action of the extract and potent (hexane) fraction was further confirmed in vivo in Wistar albino rats by evaluating them using mammalian erythrocyte micronucleus tests, DNA fragmentation, oxidative stress markers, 8-hydroxy-2-deoxyguanosine (8-OHdG), γH2AX, and histopathological lesions in the liver and hippocampus. Additionally, acute and sub-acute toxicity studies were conducted following the Organization for Economic Co-operation and Development (OECD) guidelines for rats. Furthermore, the extract was quantified and characterized by highperformance thin-layer chromatography (HPTLC), ultra-high performance liquid chromatography-mass spectroscopy (UPLC-MS), and gas chromatography-mass spectrometry (GC-MS). Results: The Piper longum ethanol extract was shown to protect plasmid pBluescript SK(-) DNA against H2O2-induced strand breaks. In human lymphocytes, the extract and hexane fraction showed a reduction in micronucleus formation (p < 0.001) and chromosomal aberrations (p < 0.01) against cyclophosphamide. Furthermore, the extract and fraction treatment, when administered at 200 mg/kg for 28 days in Wistar rats, restored cyclophosphamide-induced genomic instability by reducing micronucleus formation and DNA fragmentation; restoring redox homeostasis; decreasing 8-OHdG, a hallmark of oxidative DNA damage; reducing γH2AX, a DNA double-strand break (DSB) marker; and preserving the liver and hippocampus against histopathological lesions. The extract and fraction revealed no signs of systemic toxicity at the used doses. Piperine and piperlongumine are the major alkaloids quantified along with the presence of flavonoids in the ethanol extract and the presence of fatty acids and terpenoids in the hexane fraction of Piper longum. Conclusion: Our investigation confirms the genoprotective action of Piper longum by reducing cyclophosphamide-associated cytogenotoxicity, oxidative stress, hepato- and neurotoxicity, oxidative DNA damage, and DNA double-strand breaks. The outcomes are critical for mitigating the genotoxic effects of chemotherapy recipients, requiring further attention. [ABSTRACT FROM AUTHOR]

We previously demonstrated that prehabilitation by running on a treadmill leads to improved survival after gut ischemia reperfusion (I/R) in mice. The purpose of this research was to examine whether prehabilitation attenuates inflammatory responses after gut I/R in mice. Male C57BL/6J mice (n = 92) were assigned to the sedentary (n = 46) or the exercise (n = 46) group. The exercise group ran on a treadmill for 4 wk, while the sedentary mice did not exercise. After the 4-week pretreatment, all mice underwent gut I/R and the blood, urine, small intestine, lung, liver, and gastrocnemius were harvested prior to ischemia or at 0, 3, 6, or 24 h after reperfusion. Histologically demonstrated organ damage, cytokine levels in the blood, gut and gastrocnemius, myeloperoxidase activity in the gut, 8-hydroxy-2′-deoxyguanosine levels in urine and the gut, and adenosine triphosphate (ATP) and ATP + ADP + adenosine monophosphate levels in the gut and gastrocnemius were evaluated. The treadmill exercise reduced gut and lung injuries at 3 h and liver injury at 6 h after reperfusion. Running on the treadmill also decreased proinflammatory cytokine levels in the blood at 6 h, gut at 3 h and gastrocnemius at 6 h after reperfusion, myeloperoxidase activity in the gut prior to ischemia, and 6 h after reperfusion and the urinary 8-hydroxy-2′-deoxyguanosine level at 24 h after reperfusion, while ATP levels in exercised mice prior to ischemia and 3 h after reperfusion were increased in the intestine as compared to the levels in sedentary mice. Prehabilitation with treadmill exercise reduces inflammatory responses after gut I/R and may exert protective actions against gut I/R. [ABSTRACT FROM AUTHOR]

The extensive use of tebuconazole, an azole group fungicide, causes undesirable toxicity in non-targeted organisms, including fish in aquatic environments. We investigated metabolic responses by observing apoptosis (caspase- 3), DNA damage (8-hydroxy-2-deoxyguanosine (8-OHdG)), malondialdehyde (MDA), and antioxidants (SOD, CAT, GSH-Px) activity in Van fish kidney and muscle tissue after 24., 48., 72., and 96. h of tebuconazole exposure at a concentration of 2.5 mg/L. The obtained results indicated that caspase-3, 8-OHdG, and MDA levels significantly increased compared to the control (p < 0.05). The kidney and muscle tissues indicated a significant decrease in antioxidant enzyme activities (superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px)) compared to the control (p< 0.05). Therefore, these data may reflect one of the molecular pathways that play a role in tebuconazole toxicity. [ABSTRACT FROM AUTHOR]

IntroductionTriclosan (TCS), a widely prescribed broad-spectrum antibacterial agent, is an endocrine-disrupting chemical. The relationship and biological mechanisms between TCS exposure and breast cancer (BC) are disputed. We aimed to examine the correlation between urinary TCS exposure and BC risk and estimated the mediating effects of oxidative stress and relative telomere length (RTL) in the above association.MethodsThis case-control study included 302 BC patients and 302 healthy individuals in Wuhan, China. We detected urinary TCS, three common oxidative stress biomarkers [8-hydroxy-2-deoxyguanosine (8-OHdG), 8-iso-prostaglandin F2α (8-isoPGF2α), 4-hydroxy-2-nonenal-mercapturic acid (HNE-MA)], and RTL in peripheral blood mononuclear cells.ResultsSignificant associations were observed between log-transformed urinary concentrations of TCS, 8-OHdG, HNE-MA, 8-isoPGF2α, RTL, and BC risk, with the odds ratios (95% confidence intervals) being 1.58 (1.32–1.91), 3.08 (1.55–6.23), 3.39 (2.45–4.77), 3.99 (2.48–6.54), and 1.67 (1.35–2.09), respectively. Continuous TCS exposure was significantly positively correlated with RTL, HNE-MA, and 8-isoPGF2α (all p

Lung cancer (LC) constitutes an important cause of death among patients with Chronic Obstructive Pulmonary Disease (COPD). Both diseases may share pathobiological mechanisms related to oxidative damage and cellular senescence. In this study, the potential value of leucocyte telomere length, a hallmark of aging, and 8-OHdG concentrations, indicative of oxidative DNA damage, as risk biomarkers of LC was evaluated in COPD patients three years prior to LC diagnosis. Relative telomere length measured using qPCR and serum levels of 8-OHdG were determined at the baseline in 99 COPD smokers (33 with LC and 66 age-matched COPD without LC as controls). Of these, 21 COPD with LC and 42 controls had the biomarkers measured 3 years before. Single nucleotide variants (SNVs) in TERT, RTEL, and NAF1 genes were also determined. COPD cases were evaluated, which showed greater telomere length (p < 0.001) and increased serum 8-OHdG levels (p = 0.004) three years prior to LC diagnosis compared to the controls. This relationship was confirmed at the time of LC diagnosis. No significant association was found between the studied SNVs in cases vs. controls. In conclusion, this preliminary study shows that longer leucocyte telomere length and increased 8-OHdG serum levels can be useful as early biomarkers of the risk for future lung cancer development among COPD patients.

Oxidative stress (OS) has been linked to cell damage and chronic disease development; however, the study of psychological factors related with OS has been limited, as has its relationship with biochemical and personal variables. Therefore, the aim of this study was to evaluate the association between a wide variety of personal, psychological, and biochemical factors with OS in a sample of healthy Mexican people. A total of 134 participants, from which 70 (52%) were women, without known chronic conditions were included in the study, and the molecule 8-hydroxy-2′-deoxyguanosine (8-OHdG) was also measured as a marker of OS. We observed in the multivariate analysis of the whole sample that depressive symptoms (measured with CES-D scale) were the only psychological variable significantly associated (positively) with 8-OHdG. In addition, the following sociodemographic variables were associated with 8-OHdG: age, schooling (positively correlated), and the frequency of vitamins/antioxidant consumption (negatively correlated). The biochemical variables of erythrocytes in urine and amylase were positively correlated with 8-OHdG, while glucose was negatively correlated with it. Additional biochemical variables were associated in the multivariate analysis of each sex, including the positive correlation of LDL-cholesterol, LDH enzyme, lymphocytes, and the negative correlation of phosphorus and eosinophils in women’s samples, as well as the positive correlation of potassium, uric acid, and leucocytes in urine and the negative correlation of erythrocytes and lipase in the men’s samples. In conclusion, depression was the only psychological variable positively correlated with 8-OHdG after adjusting for confounders, and new associations with biochemical variables were found with some differences between sexes.

Ionizing radiation is strongly linked to direct or indirect DNA damage, as with the production of reactive oxygen species (ROS), which in turn produce DNA damage products, such as 8-hydroxy-2-deoxyguanosine (8-OHdG). In this study, we aimed to investigate the formation of 8-OHdG after irradiation in patients with non-small cell cancer (NSCLC) and its use as a biomarker. Sixteen patients with squamous and thirty-six patients with non-squamous pathology were included. An enzyme-linked-immunosorbent assay (ELISA) was performed before and after radiation. A dose-dependent relationship was confirmed: 8-OHdG plasma concentrations, increased in the total of NSCLC patients and specifically with a linear correlation in non-squamous pathology; in squamous histology, after an initial increase, a significant decrease followed after 20 Gy dose of irradiation. The pretreatment total irradiated tumor volume (cm3) was positively correlated with 8-OHdG levels in patients with squamous histology. When plotting the 8-OHdG plasma concentration at a 10 Gy irradiation dose to the baseline, the AUC was 0.873 (95% CI 0.614–0.984), p < 0.0001, with an associated criterion value of >1378 as a cutoff (sensitivity 72.7%, specificity 100%). When normalizing this ratio to BSA, the associated criterion cutoff value was >708 (sensitivity of 100%, specificity 80%). Lastly, 8-OHdG levels were closely related with the development of radiation-induced toxicities.

Highlights High rate of MED12 mutations and leiomyoma burden are clearly associated with myometrial oxidative stress. MED12 mutations are driven by misrepair of 8-OHdG at c.130-c.131 detected by deep sequencing analysis both in vitro and in vivo.