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Objective To investigate the changes of serum 8-hydroxy-2′-deoxyguanosine ( 8-OHdG), NTproBNP and manganese superoxide dismutase (MnSOD) in patients with heart failure (HF), and their correlation with cognitive function. Methods Ninety-six patients with HF were prospectively selected as reserach objects (HF group), meanwhile, another 96 healthy physical examinees were also enrolled as the control group. The cognitive function of the HF patients was assessed by the Montreal cognitive assessment (MoCA) score. The serum levels of 8-OHdG, NT-proBNP and MnSOD were compared between the two groups, and patients with different cognitive status at admission. The correlation between the levels of the above three serum markers and MoCA score was also analyzed. The diagnostic value of the above three serum indicators for cognitive dysfunction at admission was analyzed. Results The levels of serum 8-OHdG and NT-proBNP in patients with HF at admission were significantly higher than those in the control group, while the level of serum MnSOD was significantly lower (all P<0. 01). The levels of serum 8-OHdG and NT-proBNP in HF patients with cognitive dysfunction were significantly higher than those in HF patients with normal cognition funtion, while the level of serum MnSOD was significantly lower (all P< 0. 01). For the HF patients at admission, the levels of serum 8-OHdG and NT-proBNP were both positively correlated with the MoCA score, while the level of serum MnSOD was negatively correlated with the MoCA score (all P<0. 05). In the diagnosis of cognitive dysfunction among HF patients, the area under the curve, sensitivity, and specificity of the combination of serum 8-OHdG, NT-proBNP, and MnSOD levels at admission were all significantly higher than those by using any single of the three indicators. Conclusion The serum levels of 8-OHdG, NT-proBNP and MnSOD are closely related to complicated cognitive dysfunction in patients with HF. The joint detection of the three markers significantly increases the diagnostic value of cognitive dysfunction in HF patients, which could provide references for clinical treatment. [ABSTRACT FROM AUTHOR]

Objectives: 8-hydroxydeoxyguanosine (8-OHdG) and Malondialdehyde (MDA) are commonly used as markers to evaluate oxidative DNA and Lipid damage in disorders including chronic inflammatory diseases. Superoxide dismutase (SOD) and glutathione peroxidase (GPx) protect tissues against oxidative injury from free oxygen radicals generated by various metabolic processes. The aim of this study was to evaluate 8-OHdG and MDA levels, and SOD and GPx activities in whole saliva of patients with peri-implant diseases. Materials and methods: A cross-sectional study was conducted on a sum of 60 age gender balanced; peri-implantitis (n = 20), peri-mucositis (n = 20) and healthy (n = 20) individuals. Unstimulated whole saliva samples were collected and to determine the clinical condition of each subject; the plaque index (PI), gingival index (GI), peri-implant probing pocket depth (PIPD), peri-implant presence of bleeding on probing (BOP) (with/without suppuration) and radiographic signs of crestal bone loss (BL) were measured. The salivary 8-OHdG level was measured using the ELISA method. SOD, GPx activities and MDA levels were determined spectrophotometrically. Results: A total of 60 individuals had evaluations of 318 implants. In comparison to the peri-mucositis and peri-implantitis groups, the healthy group had significantly lower PI and GI scores (p < 0.001). The PIPD value differed amongst the groups, with the peri-implantitis group having the highest value (p < 0.001). Compared to the peri-mucositis and control groups, the peri-implantitis group had a significantly higher BL score (p < 0.001 and p < 0.001, respectively). The peri-implantitis group showed a significantly higher 8-OHdG level (p < 0.001; p < 0.001 respectively) than the peri-mucositis and control groups. Compared to the peri-mucositis and control groups, the peri-implantitis group had a significantly higher MDA level (p < 0.001 and p < 0.001, respectively). The peri-implantitis group had a significantly higher SOD level (p < 0.001 and p < 0.001, respectively) in comparison to the peri-mucositis and control groups. There was no significant difference in GPx levels between the peri-mucositis and control groups (p > 0.05), while the peri-implantitis group had significantly lower GPx levels than the peri-mucositis and control groups (p < 0.001 and p < 0.001, respectively). Conclusions: Elevated levels of oxidative stress in saliva may indicate the onset of pathological bone loss surrounding the implant and may be an indication of peri-implantitis. Clinical relevance: In peri-implant diseases, changes may occur in the levels of 8-OHdG, MDA, SOD and GPx in saliva, which may lead to a deterioration in the oxidant/antioxidant balance. [ABSTRACT FROM AUTHOR]

[Objectives] To analyze the relationship between serum 8-hydroxydeoxyguanosine (8-OHdG), heart fatty acid-binding protein (H-FABP), C-reactive protein (CRP) levels and clinical efficacy and short-term prognosis in patients with ischemic cardiomyopathy. [Methods] The clinical data of 100 patients with ischemic cardiomyopathy from October 2021 to November 2022 w'ere retrospectively analyzed, and the serum levels of 8-OHdG, H-FABP and CRP were compared before and one week after treatment. The patients were followed up for 12 months after discharge, and the incidence of major adverse cardiovascular events (MACE) was counted during the follow-up period. Univariate and multivariate Logistic regression analysis were used to analyze the prognostic factors of patients with ischemic cardiomyopathy in the near future, and the predictive value of serum 8-OHdG, H-FABP and CRP levels for the prognosis of patients was evaluated by ROC curve. [Results] After 1 week of treatment, the serum levels of 8-OHdG, H-FABP and CRP in patients with ischemic cardiomyopathy were significantly lower than those before treatment (P < 0.05). During the follow'-up period, 34 patients developed MACE; the serum levels of 8-OHdG, H-FABP and CRP in the MACE group were higher than those in the non-MACE group, and the differences were statistically significant (P < 0. 05). Multivariate Logistic regression analysis show'ed that 8-OHdG, H-FABP and CRP w'ere the risk factors of MACE in patients w'ith ischemic cardiomyopathy (P<0.05). ROC curve analysis showed that the combined prediction of 8-OHdG, H-FABP and CRP for MACE in patients with ischemic cardiomyopathy was higher than that of CRP, H-FABP and 8-OHdG alone (P <0.05). [Conclusions] 8-OHdG, H-FABP and CRP are closely related to the clinical efficacy and short-term prognosis of patients with ischemic cardiomyopathy, and the detection of serum 8-OHdG, H-FABP and CRP levels can help to evaluate the clinical efficacy and short-term prognosis of patients with ischemic cardiomyopathy. [ABSTRACT FROM AUTHOR]

Aim To investigate the relationship between serum 8-hydroxydeoxyguanosine (8-OHdG ), chemokine C-X3-C ligand 1 (CX3CL1) and cognitive dysfunction in patients with cerebral small vessel disease (CSVD). Methods 128 patients with CSVD admitted to our hospital from May 2021 to May 2022 were selected and divided into cognitive impairment group and non-cognitive impairment group based on the Montreal cognitive assessment scale (MoCA) scores. The relationship between serum 8-OHdG, CX3CL1 levels and the MoCA scores of CSVD patients was investigated by Pearson correlation analysis, Logistic regression analysis was used to analyze the influencing factors of cognitive impairment in patients with CSVD, and ROC curves were drawn to study the predictive efficacy of serum 8-OHdG and CX3CL1 on cognitive impairment in CSVD patients. Results The serum 8-OHdG and CX3CL1 levels of patients with cognitive impairment were higher than those of non-cognitive impairment group. However, their MoCA scores were lower than those of non-cognitive impairment group (P<0. 05). Serum 8-OHdG and CX3CL1 levels were negatively correlated with MoCA scores (r = -0. 715 and -0. 413, P<0. 05). Serum 8-OHdG level was higher in severe cognitive impairment group than that of moderate cognitive impairment group and mild cognitive impairment group (P<0. 05), and it was higher in moderate cognitive impairment group than that of mild cognitive impairment group (P<0. 05). Serum of CX3CL1 level was higher in severe cognitive impairment group than that in moderate cognitive impairment group and mild cognitive impairment group (P<0. 05), and it was higher in moderate cognitive impairment group than that in mild cognitive impairment group (P< 0. 05). The area under the ROC curve (AUC) of 8-OHdG for the diagnosis of cognitive impairment in CSVD patients was 0. 866, with sensitivity and specificity of 76. 53% and 80. 00%, respectively (P<0. 05); The AUC of CX3CL1 for the diagnosis of cognitive impairment in CSVD patients was 0. 868, with sensitivity and specificity of 86. 73% and 80. 00%, respectively (P<0. 05); The AUC of the combination of 8-OHdG and CX3CL1 for the diagnosis of cognitive impairment in CSVD patients was 0. 922, with sensitivity and specificity of 88. 78% and 86. 67%, respectively (P<0. 05). Serum 8- OHdG>2. 69 μg / L and CX3CL1 >179. 18 pg / L were both influencing factors for cognitive impairment in CSVD patients (P<0. 05). Conclusion The levels of serum 8-OHdG and CX3CL1 are positively correlated with cognitive impairment in CSVD patients, and both can serve as auxiliary indicators for predicting cognitive impairment in CSVD patients. [ABSTRACT FROM AUTHOR]

Metabolic syndrome (MetS) is a cluster of metabolic abnormalities affecting ~25% of adults and is linked to chronic diseases such as cardiovascular disease, cancer, and neurodegenerative diseases. Oxidative stress and inflammation are key drivers of MetS. Hesperidin, a citrus bioflavonoid, has demonstrated antioxidant and anti-inflammatory properties; however, its effects on MetS are not fully established. We aimed to determine the optimal dose of hesperidin required to improve oxidative stress, systemic inflammation, and glycemic control in a novel mouse model of MetS. Male 5-week-old C57BL/6 mice were fed a high-fat, high-salt, high-sugar diet (HFSS; 42% kcal fat content in food and drinking water with 0.9% saline and 10% high fructose corn syrup) for 16 weeks. After 6 weeks of HFSS, mice were randomly allocated to either the placebo group or low- (70 mg/kg/day), mid- (140 mg/kg/day), or high-dose (280 mg/kg/day) hesperidin supplementation for 12 weeks. The HFSS diet induced significant metabolic disturbances. HFSS + placebo mice gained almost twice the weight of control mice (p < 0.0001). Fasting blood glucose (FBG) increased by 40% (p < 0.0001), plasma insulin by 100% (p < 0.05), and HOMA-IR by 150% (p < 0.0004), indicating insulin resistance. Hesperidin supplementation reduced plasma insulin by 40% at 140 mg/kg/day (p < 0.0001) and 50% at 280 mg/kg/day (p < 0.005). HOMA-IR decreased by 45% at both doses (p < 0.0001). Plasma hesperidin levels significantly increased in all hesperidin groups (p < 0.0001). Oxidative stress, measured by 8-OHdG, was increased by 40% in HFSS diet mice (p < 0.001) and reduced by 20% with all hesperidin doses (p < 0.005). In conclusion, hesperidin supplementation reduced insulin resistance and oxidative stress in HFSS-fed mice, demonstrating its dose-dependent therapeutic potential in MetS. [ABSTRACT FROM AUTHOR]

Objective: To investigate the effects of cell passage number on the establishment of an oxidative stress model in human colon adenocarcinoma cells (Caco-2) caused by tert-butyl hydroperoxide (t-BHP). Methods: First, by applying various t-BHP concentrations (1, 2 and 3 mmol/L) to the F15 generation of Caco-2 cells for 1, 2, 3, 4, 5 and 6 hours, the content of malondialdehyde (MDA) and 8-hydroxydeoxyguanosine (8-OHdG) in different treatment groups were measured to determine the basic conditions for constructing the oxidative stress model of Caco-2 cells. Then, based on the fundamental parameters, the effect of cell passage number (F14, F15, F18, F19 and F20) on the development of oxidative stress model was investigated using the content of 8-OHdG as an index. Results: When exposed to 1, 2 and 3 mmol/L of t-BHP for 3 to 6 hours, the oxidative stress model of Caco-2 cells from the F15 generation could be established steadily. The content of 8-OHdG in Caco-2 cells of the F14, F15 and F18 generations was significantly higher than that in control group (which had not been treated with t-BHP) after being exposed to 2.0 mmol/L t-BHP for 5 hours (P

Polycyclic aromatic hydrocarbons (PAHs) have been reported to cause oxidative stress in metabolic processes. This study aimed to evaluate the relationship between exposure to PAHs, including benzo[a]pyrene (BaP) and 1-nitropyrene (1-NP), in the atmosphere and oxidative stress levels in the human body. This study included 44 Korean adults who lived in Cheongju, Republic of Korea. Atmospheric BaP and 1-NP concentrations and urinary 6-hydroxy-1-nitropyrene (6-OHNP), N-acetyl-1-aminopyrene (1-NAAP), and 1-hydroxypyrene (1-OHP) concentrations were measured. The oxidative stress level was assessed by measuring urinary thiobarbituric acid-reactive substances (TBARS) and 8-hydroxydeoxyguanosine (8-OHdG) concentrations. Urinary TBARS and 6-OHNP concentrations significantly differed between winter and summer. BaP exposure was significantly associated with urinary 8-OHdG concentrations in summer. However, atmospheric 1-NP did not show a significant correlation with oxidative stress marker concentrations. Urinary 1-NAAP concentration was a significant determinant for urinary 8-OHdG concentration in summer. Oxidative stress in the body increases in proportion to inhalation exposure to BaP, and more 8-OHdG is produced in the body as the amount of 1-NP, which is metabolized to 1-AP or 1-NAAP, increases. [ABSTRACT FROM AUTHOR]

Post-COVID conditions are defined as the continuation of the symptoms of Coronavirus Disease 2019 (COVID-19) 3 months after the initial Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection, with no other explanation. Post-COVID conditions are seen among 30%–60% of patients with asymptomatic or mild forms of COVID-19. The underlying pathophysiological mechanisms of post-COVID conditions are not known. In SARS-CoV-2 infection, activation of the immune system leads to increased production of reactive oxygen molecules, depleted antioxidant reserve, and finally occurrence of oxidative stress. In oxidative stress conditions, DNA damage increases and DNA repair systems impair. In this study, glutathione (GSH) level, glutathione peroxidase (GPx) activity, 8-hydroxydeoxyguanosine (8-OHdG) level, basal, induced, and post-repair DNA damage were investigated in individuals suffering from post-COVID conditions. In the red blood cells, GSH levels and GPx activities were measured with a spectrophotometric assay and a commercial kit. Basal, in vitro H2O2 (hydrogen peroxide)-induced, and post-repair DNA damage (DNA damage after a repair incubation following H2O2-treatment, in vitro) were determined in lymphocytes by the comet assay. The urinary 8-OHdG levels were measured by using a commercial ELISA kit. No significant difference was found between the patient and control groups for GSH level, GPx activity, and basal and H2O2-induced DNA damage. Post-repair DNA damage was found to be higher in the patient group than those in the control group. Urinary 8-OHdG level was lower in the patient group compared to the control group. In the control group, GSH level and post-repair DNA damage were higher in the vaccinated individuals. In conclusion, oxidative stress formed due to the immune response against SARS-COV-2 may impair DNA repair mechanisms. Defective DNA repair may be an underlying pathological mechanism of post-COVID conditions. [ABSTRACT FROM AUTHOR]

Particulate matter 2.5 (PM2.5) induces lung injury by increasing the generation of reactive oxygen species (ROS) and inflammation. ROS aggravates NLRP3 inflammasome activation, which activates caspase-1, IL-1β, and IL-18 and induces pyroptosis; these factors propagate inflammation. In contrast, treatment with exogenous 8-hydroxydeoxyguanosine (8-OHdG) decreases RAC1 activity and eventually decreases dinucleotide phosphate oxidase (NOX) and ROS generation. To establish modalities that would mitigate PM2.5-induced lung injury, we evaluated whether 8-OHdG decreased PM2.5-induced ROS generation and NLRP3 inflammasome activation in BEAS-2B cells. CCK-8 and lactate dehydrogenase assays were used to determine the treatment concentration. Fluorescence intensity, Western blotting, enzyme-linked immunosorbent assay, and immunoblotting assays were also performed. Treatment with 80 μg/mL PM2.5 increased ROS generation, RAC1 activity, NOX1 expression, NLRP3 inflammasome (NLRP3, ASC, and caspase-1) activity, and IL-1β and IL-18 levels in cells; treatment with 10 μg/mL 8-OHdG significantly attenuated these effects. Furthermore, similar results, such as reduced expression of NOX1, NLRP3, ASC, and caspase-1, were observed in PM2.5-treated BEAS-2B cells when treated with an RAC1 inhibitor. These results show that 8-OHdG mitigates ROS generation and NLRP3 inflammation by inhibiting RAC1 activity and NOX1 expression in respiratory cells exposed to PM2.5. [ABSTRACT FROM AUTHOR]

This work showed that radiological abnormalities and reduction in ventilatory functions among silica-exposed workers was mediated through oxidative stress, evidenced by increased serum MDA level, indicating lipid peroxidation, and increased serum 8-HdG indicating oxidative DNA damage. Consumption of GPx enzyme occured to balance the oxidative effects of the free radicals. Objective: To investigate the changes of the ventilatory function tests and the oxidative stress biomarkers among silica-exposed foundry workers. Methods: The exposed group included 70 workers in an iron foundry. The nonexposed group included 40 subjects from Kasralainy outpatient clinic. Both groups were subjected to history taking, clinical examination, chest radiograph, spirometry, urinary silica, serum malondialdehyde (MDA), glutathione peroxidase (GPx), and 8-hydroxydeoxyguanosine (8-HdG). Results: Higher urinary silica, serum MDA and serum 8-HdG, whereas lower serum GPx and ventilatory functions were detected in the exposed group compared with the controls. All parameters correlated with urinary silica. The exposed silicotic subgroup had increased work duration, urinary silica, serum MDA, and serum 8-HdG, and decreased serum GPx and ventilatory functions compared with non-silicotic subgroup. Conclusion: Oxidative stress biomarkers were abnormal with impairment of ventilatory functions among silica-exposed workers. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Orofacial Orthopedics/Fortschritte der Kieferorthopadie is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

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

8-hydroxydeoxyguanosine (8-OHdG) in human urine is a marker reflecting oxidative stress and DNA oxidative damage. People spend 80%-90% of their life indoors; therefore, indoor air quality is directly related to human health. In this paper, the urinary 8-OHdG levels were presented in populations grouped by different demographic characteristics, lifestyle, occupational exposure, and health status, and elucidated indoor pollutants affecting human urinary 8-OHdG level, such as pollutants from outdoor sources, smoking, indoor combustion and cooking fumes, the chemicals in interior decoration materials, and building foundation soils. The article aims to provide a theoretical basis for predicting the impact of indoor air pollution on human health (DNA oxidative damage and related diseases) by measuring the concentration of 8-OHdG in human urine.

Polycyclic aromatic hydrocarbons (PAHs) have been reported to cause oxidative stress in metabolic processes. This study aimed to evaluate the relationship between exposure to PAHs, including benzo[a]pyrene (BaP) and 1-nitropyrene (1-NP), in the atmosphere and oxidative stress levels in the human body. This study included 44 Korean adults who lived in Cheongju, Republic of Korea. Atmospheric BaP and 1-NP concentrations and urinary 6-hydroxy-1-nitropyrene (6-OHNP), N-acetyl-1-aminopyrene (1-NAAP), and 1-hydroxypyrene (1-OHP) concentrations were measured. The oxidative stress level was assessed by measuring urinary thiobarbituric acid-reactive substances (TBARS) and 8-hydroxydeoxyguanosine (8-OHdG) concentrations. Urinary TBARS and 6-OHNP concentrations significantly differed between winter and summer. BaP exposure was significantly associated with urinary 8-OHdG concentrations in summer. However, atmospheric 1-NP did not show a significant correlation with oxidative stress marker concentrations. Urinary 1-NAAP concentration was a significant determinant for urinary 8-OHdG concentration in summer. Oxidative stress in the body increases in proportion to inhalation exposure to BaP, and more 8-OHdG is produced in the body as the amount of 1-NP, which is metabolized to 1-AP or 1-NAAP, increases.

Urinary 8-hydroxydeoxyguanosine (8-OHdG) level is an oxidative stress marker in patients with cancer; however, little is currently known about the clinical relevance of urinary 8-OHdG levels in patients with prostate cancer at diagnosis. Voided urine samples were collected from patients at the time of prostate biopsy and stored at -80˚C after centrifugation. All of the patients were classified according to histology of the biopsy. Once the patients were diagnosed with prostate cancer, the standard of care and treatments were administered according to the standard guidelines. The association between clinicopathological parameters and urinary 8-OHdG and N-terminal telopeptide (NTx) levels were explored. A total of 409 patients received prostate biopsy, of which 190 were benign, 41 were diagnosed with prostatitis and 178 were diagnosed with prostate cancer. The urinary 8-OHdG/creatinine ratio was marginally associated with prostate size (P=0.052) but not with serum prostate-specific antigen levels (P=0.707). With correction for prostate size, the ratio of urinary 8-OHdG/creatinine was significantly higher in patients with prostate cancer than those without malignancy (P=0.004). Moreover, urinary 8-OHdG levels were weakly associated with urinary NTx levels (r2=0.04, P=0.009). In conclusion, urinary 8-OHdG levels normalized for prostate volume may reflect prostate cancer risk and could be used to predict prostate cancer aggressiveness. [ABSTRACT FROM AUTHOR]

Oxidative stress is a condition caused by an imbalance in the occurrence of reactive oxygen species in the cells and tissues of organisms. An ultra-performance liquid chromatography–electrospray ionization tandem mass spectrometry (UPLC–ESI–MS/MS) method was developed for the simultaneous determination of two oxidative stress biomarkers, 8-hydroxydeoxyguanosine (8OHDG) and dityrosine (DIY), in the gills, skin, dorsal fin, and liver tissue of Atlantic salmon (Salmo salar) parr. The use of target analyte-specific 13C and 15N internal standards allowed quantification of each target analyte to be performed through the standard solvent calibration curve. The relative recoveries [mean ± (relative standard deviation%)] of 8OHDG and DIY were 101 ± 11 and 104 ± 13% at a fortified concentration of 10 ng/mL (8OHDG) and 500 ng/mL (DIY), respectively, ensuring the accuracy of the extraction and quantification. The chromatographic separation was carried out using a gradient elution program with a total run time of 5 min. The limits of detection (LODs) were 0.11 and 1.37 ng/g wet weight (w.w.) for 8OHDG and DIY, respectively. To demonstrate the applicability of the developed method, it was applied in 907 tissue samples that were collected from Atlantic salmon parr individuals reared in an experimental land-based recirculating aquaculture system (RAS) treated with peracetic acid. Moreover, the possibility of using the dorsal fin as an alternative matrix for the minimally invasive assessment of oxidative stress in Atlantic salmon parr was introduced. To our knowledge, 8OHDG and DIY were used for the first time as biomarkers for biomonitoring the fish health (oxidative stress) of Atlantic salmon parr in RAS. [ABSTRACT FROM AUTHOR]

Selenoproteins and selenium (Se) are essential for thyroid hormone synthesis, metabolism and thyroid gland functions. The human thyroid gland is one of the organs vulnerable to tissue- -specific autoimmune diseases. The aim of this study was to investigate roles of Se and several selenoproteins, including selenoprotein P (SePP), glutathione peroxidase-3 (GPx3), thioredoxin reductase (TrxR), type 1 iodothyronine deiodinase (DI1), selenoprotein W (SelW), selenoprotein H (SelH), and oxidative stress in etiopathogenesis of Hashimoto thyroiditis. A total of 40 patients with Hashimoto thyroiditis and 42 healthy controls were included in the study. Serum Se levels were measured by inductively coupled plasma optical emission spectrometry (ICP-OES). 8-hydroxydeoxyguanosine (8-OHdG), SePP, SelW, SelH, GPx-3, TrxR, and DI1 levels were determined by enzyme-linked immunosorbent assay (ELISA) kits. Se levels were significantly decreased, but plasma SelH, 8-OHdG levels, and TrxR activities were significantly increased in the Hashimoto thyroiditis group. Plasma SePP levels, GPx3and DI1 activities did not significantly changed in Hashimoto thyroiditis patients. Changes in circulating Se and selenoprotein levels/activities, together with increased oxidative stress, might have important impact on the etiopathogenesis of Hashimoto thyroiditis. [ABSTRACT FROM AUTHOR]

Copyright of Folia Medica Indonesiana (2355-8393) is the property of Universitas Airlangga and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Particulate matter 2.5 (PM2.5) induces lung injury by increasing the generation of reactive oxygen species (ROS) and inflammation. ROS aggravates NLRP3 inflammasome activation, which activates caspase-1, IL-1β, and IL-18 and induces pyroptosis; these factors propagate inflammation. In contrast, treatment with exogenous 8-hydroxydeoxyguanosine (8-OHdG) decreases RAC1 activity and eventually decreases dinucleotide phosphate oxidase (NOX) and ROS generation. To establish modalities that would mitigate PM2.5-induced lung injury, we evaluated whether 8-OHdG decreased PM2.5-induced ROS generation and NLRP3 inflammasome activation in BEAS-2B cells. CCK-8 and lactate dehydrogenase assays were used to determine the treatment concentration. Fluorescence intensity, Western blotting, enzyme-linked immunosorbent assay, and immunoblotting assays were also performed. Treatment with 80 μg/mL PM2.5 increased ROS generation, RAC1 activity, NOX1 expression, NLRP3 inflammasome (NLRP3, ASC, and caspase-1) activity, and IL-1β and IL-18 levels in cells; treatment with 10 μg/mL 8-OHdG significantly attenuated these effects. Furthermore, similar results, such as reduced expression of NOX1, NLRP3, ASC, and caspase-1, were observed in PM2.5-treated BEAS-2B cells when treated with an RAC1 inhibitor. These results show that 8-OHdG mitigates ROS generation and NLRP3 inflammation by inhibiting RAC1 activity and NOX1 expression in respiratory cells exposed to PM2.5.

Oxidative stress is a condition caused by an imbalance in the occurrence of reactive oxygen species in the cells and tissues of organisms. An ultra-performance liquid chromatography–electrospray ionization tandem mass spectrometry (UPLC–ESI–MS/MS) method was developed for the simultaneous determination of two oxidative stress biomarkers, 8-hydroxydeoxyguanosine (8OHDG) and dityrosine (DIY), in the gills, skin, dorsal fin, and liver tissue of Atlantic salmon (Salmo salar) parr. The use of target analyte-specific 13C and 15N internal standards allowed quantification of each target analyte to be performed through the standard solvent calibration curve. The relative recoveries [mean ± (relative standard deviation%)] of 8OHDG and DIY were 101 ± 11 and 104 ± 13% at a fortified concentration of 10 ng/mL (8OHDG) and 500 ng/mL (DIY), respectively, ensuring the accuracy of the extraction and quantification. The chromatographic separation was carried out using a gradient elution program with a total run time of 5 min. The limits of detection (LODs) were 0.11 and 1.37 ng/g wet weight (w.w.) for 8OHDG and DIY, respectively. To demonstrate the applicability of the developed method, it was applied in 907 tissue samples that were collected from Atlantic salmon parr individuals reared in an experimental land-based recirculating aquaculture system (RAS) treated with peracetic acid. Moreover, the possibility of using the dorsal fin as an alternative matrix for the minimally invasive assessment of oxidative stress in Atlantic salmon parr was introduced. To our knowledge, 8OHDG and DIY were used for the first time as biomarkers for biomonitoring the fish health (oxidative stress) of Atlantic salmon parr in RAS.

DPM (diesel particulate matter) is ubiquitously present in the mining environment and is known for mutagenicity and carcinogenicity to humans. However, its health effects in surface coal mines are not well studied, particularly in India. In this study, DPM exposure and corresponding exposure biomarkers were investigated in four different surface coal mines in Central India. To document and evaluate the DPM exposure in surface coal miners, we characterized 1-NP (1-nitropyrene) in the mining environment as surrogate for DPM using Sioutas Cascade Impactor. Exposure biomarkers were analyzed by collecting post work shift (8-h work shift) urine samples and determining the concentrations of 1-aminopyrene (1-AP) as a metabolite of 1-NP and 8-hydroxydeoxyguanosine (8OHdG) as DNA damage marker. We observed high concentration of 1-NP (7.13–52.46 ng/m3) in all the mines compared with the earlier reported values. The average creatinine corrected 1-AP and 8OHdG levels ranged 0.07–0.43 μ g/g and 32.47–64.16 μ g/g, respectively, in different mines. We found 1-AP in majority of the mine workers' urine (55.53%) and its level was higher than that reported for general environmental exposure in earlier studies. Thus, the study finding indicates occupational exposure to DPM in all the four mines. However, the association between 1-NP level and exposure biomarkers (1-AP and 8OHdG) was inconsistent, which may be due to individual physiological variations. The data on exposure levels in this study will help to understand the epidemiological risk assessment of DPM in surface coal miners. Further biomonitoring and cohort study are needed to exactly quantify the occupational health impacts caused by DPM among coal miners. [ABSTRACT FROM AUTHOR]

This study aimed to investigate the relationship between endogenous antioxidant system, 8-hydroxydeoxyguanosine adduct (8-OHdG) repair, and apoptosis in mice treated with chromium(VI) alone and in the presence of the antigenotoxic compound (-)-epigallocatechin-3-gallate (EGCG). Groups of 5 Hsd:ICR male mice were divided and treated as follows: (1) control, vehicle only; (2) EGCG, 8.5 mg/kg by gavage alone; (3) CrO3, 20 mg/kg intraperitoneally alone; and (4) EGCG combined with CrO3, EGCG was administered 4 hr prior to CrO3. Peripheral blood parameters were analyzed before treatment administration (time 0), and 48 hr after exposure. The administration of EGCG increased 8-OHdG levels and superoxide dismutase (SOD) activity. Treatment with CrO3 increased number of micronucleus (MN) presence, elevated apoptotic/necrotic cells frequencies, decreased 8-OHdG levels, diminished total antioxidant capacity (TAC), increased glutathione (GSH) total levels, and lowered SOD activity. Administration of EGCG prior to treatment with CrO3 resulted in lower concentrations of MN, reduced apoptotic and necrotic cell number, and restored TAC and SOD activity to control levels. It is conceivable that the dose of EGCG plays an important role in the genotoxic damage protection pathways. Thus, this study confirms the action of EGCG as an antigenotoxic agent against chromium(VI)-induced oxidative insults and demonstrates potential protective pathways for EGCG actions to counteract genotoxic damage induced by this metal. [ABSTRACT FROM AUTHOR]

ABSTRACT Background and Objectives: Oxidative stress is a common mediator in pathogenicity of established cardiovascular risk factors. The purpose of this study was to determine effects of selected aerobic training on some oxidative stress indicators in sedentary elderly women. Methods: In this quasi-experimental study, 21 participants (age range: 60-70 years) were selected by convenience sampling and then randomly assigned to an exercise group (n=11) and a control group (n=10). Aerobic exercise was performed at 50-70% of heart rate reserve for 45-60 minutes per session, three sessions a week, for eight weeks. Blood samples were taken at baseline and 24 hours after the last training session. Within-group and between-group differences were assessed using paired sample t-test and independent t-test, respectively. Statistical significance level was set at 0.05. Results: Weight, body mass index and body fat percentage decreased significantly after the exercise intervention (P

Gliomas are one of the most aggressive brain tumors with a poor prognosis in the central nervous system. Bexarotene is a third-generation retinoid X receptor agonist that is promising in the treatment of both cancer and neurodegenerative diseases. In this study, we aimed to investigate the cytotoxic and anti-proliferative effects of bexarotene in C6 glioma cells through the PPARγ/NF-κB pathway. In the study, first cytotoxic bexarotene concentrations for C6 cells were detected, and then apoptosis profile, reactive oxygen species (ROS), total antioxidant (TAS), 8-hydroxy-2'-deoxyguanosine (8-OHdG) and nuclear factor-κB (NF-κB) levels in the cells were determined. In addition, peroxisome proliferator-activated receptor γ (PPARγ) mRNA expression analysis was carried out. As a result, we detected concentration- and time-dependent antiproliferative effects of bexarotene on C6 cells. We found that bexarotene treatment decreased NF-κB and TAS levels and increased PPARγ and 8-OHdG levels in C6 cells. Bexarotene enhanced PPARγ expression in a dose-dependent manner when compared to the control group (P < 0.01). Furthermore, we determined that bexarotene-induced apoptotic C6 cells enhanced through Annexin V-FITC/PI staining and caspase-3/-7 activation analyses since phosphatidylserine level on the outer surface of the cell membrane and caspase-3/-7 activities were increased in the cells treated with bexarotene. In conclusion, bexarotene treatment in C6 glioma cells could modulate apoptosis profile, DNA damage, ROS production, and reduction of TAS levels through inhibition of NF-κB by enhancing PPARγ expression. [ABSTRACT FROM AUTHOR]

Wintering is associated with distress to humans who work in the isolated and confined environment of Antarctica and yoga has been proved helpful for coping with stress. Therefore, a study was conducted on 14 winter expedition members of Indian Scientific Antarctic Expedition (2016) to find out the effects of yoga on stress-related markers. Participants were divided into yoga, and control (non-yoga) groups. The yoga group practiced yoga for 10 months (from January to October 2016) daily in the morning for an hour. The Resilience test questionnaire was administrated at baseline and endpoint of the study. Blood samples were collected during the study at different intervals for the estimation of 8-hydroxydeoxyguanosine (8-OHdG), brain-derived neurotrophic factor (BDNF), serotonin and cortisol using ELISA. A trend of improvement was observed in the resilience test score in the yoga group. From January to October, 8-OHdG serum values in the yoga group declined by 55.9% from 1010.0 ± 67.8 pg/mL to 445.6 ± 60.5 pg/mL (Mean ± SD); in the control group, the decline was 49.9% from 1060.4 ± 54.6 pg/mL to 531.1 ± 81.8 pg/mL. In serotonin serum levels in the yoga group, there was a 3.1% increase from 6.4 ± 1.6 ng/mL to 6.6 ± 0.4 ng/mL while no increase was noticed in the control group. Cortisol values in the yoga group decreased by 19.9% from 321.0 ± 189.6 ng/mL to 257.1 ± 133.8 ng/mL; in the control group it increased by 2.8% from 241.2 ± 51.8 ng/mL to 247.8 ± 90.9 ng/mL. It could be concluded from the present study that following 10 months yoga practice may be useful for better resilience and management of stress-related blood markers for the polar sojourners. [ABSTRACT FROM AUTHOR]

The aim of the present study was to determine whether urinary 8-hydroxydeoxyguanosine (8-OHdG), which is a marker of oxidative stress, can predict future cardiovascular death in patients with acute coronary syndrome (ACS). A total of 551 consecutive patients with ACS who underwent admission urinary 8-OHdG measurements were enrolled in this study. The patients were divided into 2 groups according to the optimal cutoff value of admission urinary 8-OHdG determined by a receiver-operating characteristics curve for the prediction of cardiovascular death: a high admission urinary 8-OHdG group, 169 patients with admission urinary 8-OHdG ≥ 17.92 ng/mg creatinine; and a low admission urinary 8-OHdG group, 382 patients with admission urinary 8-OHdG < 17.92 ng/mg creatinine. The patients were followed up for a median period of 34 months. The primary and secondary end points were the incidence of cardiovascular death and major cardiovascular events (MACE) composed of cardiovascular death, non-fatal myocardial infarction, or urgent hospitalization for heart failure. Of the 551 patients, cardiovascular deaths and MACE occurred in 14 (2.5%) and 35 (6.4%), respectively. The Kaplan–Meier estimate of the event-free rate revealed cardiovascular deaths and MACE were more likely in the high admission 8-OHdG group than in the low admission 8-OHdG group (log rank, both P < 0.001). Multiple adjusted Cox proportional hazards analysis indicated that high admission urinary 8-OHdG was an independent predictor of cardiovascular death (hazard ratio [HR] 7.642, P = 0.011) and MACE (HR 2.153, P = 0.049). High admission urinary 8-OHdG levels predict cardiovascular mortality after adjustment in patients with ACS. [ABSTRACT FROM AUTHOR]

Objective: A growing body of evidence shows a close relationship between oxidative stress and autoimmune conditions such as Hashimoto's thyroiditis (HT). Among different markers of oxidative damage, 8-hydroxydeoxyguanosine (8-OHdG) is a ubiquitous marker and broadly used in research studies. Therefore, this study aimed to measure the level of 8-OHdG in the sera of patients with HT and healthy control (HC) participants. Material and Methods: In this study, patients were diagnosed with clinical (n=23) and subclinical (n=25) hypothyroidism because of HT and compared with 35 healthy participants. 8-OHdG was measured using enzyme-linked immunosorbent assay in patients and HC participants. Results: No significant difference was observed in the mean serum 8-OHdG levels between patients and HC participants. Conclusion: The results of this preliminary study do not support the fact that the serum level of 8-OHdG is a biomarker of oxidative stress in patients with HT. However, more detailed studies are needed to reveal the exact role of 8-OHdG in this autoimmune disease of the thyroid gland. [ABSTRACT FROM AUTHOR]

Cigarette smoke is a known risk factor for urothelial carcinoma (UC). However, there is limited information about the distributions and effects of volatile organic compounds (VOCs) on smoking-related UC risk. With this hospital-based case-control study, we explored the associations between urinary levels of cotinine and VOC metabolites (acrylamide, 1,3-butadiene, and benzene) and the risk of UC. Urological examinations and pathological verifications were used to confirm the diagnoses of UC. All study participants provided smoking-related information via questionnaires and face-to-face interviews; they also provided urine samples for the measurement of VOC metabolites, cotinine, and 8-hydroxydeoxyguanosine (8-OHdG), which was used as an indicator of oxidative stress. We applied multiple logistic regression analysis to estimate the risk of UC, and we found that levels of urinary cotinine and 8-OHdG were higher in the UC group than in the control group. Furthermore, urinary levels of VOC metabolites, including N-acetyl-S-(2-carbamoylethyl)-L-cysteine (AAMA), N-acetyl-S-(2-carbamoyl-2-hydroxyethyl)-L-cysteine, N-acetyl-S-(4-hydroxy-2-buten-1-yl)-L-cysteine-3, trans,trans-muconic acid (t,t-MA), and S-phenylmercapturic acid (SPMA), increased with increasing levels of urinary cotinine. After adjusting for potential risk factors, dose–response relationships were observed between UC risk and urinary levels of AAMA, t,t-MA, SPMA, and 8-OHdG. Participants with high urinary levels of cotinine, AAMA, t,t-MA, SPMA, and 8-OHdG had risks of UC that were 3.5- to 6-fold higher than those of participants with lower levels. Future, large-scale investigations of the risks of UC should be explored, and repeated measurement of VOC metabolites should be assessed. [ABSTRACT FROM AUTHOR]

Aims: In overactive bladder (OAB) research, different biomarkers have been proposed as diagnostic tools and may be used to create individual patient profiles. Assessing the diagnostic performance of biomarkers would better outline their utility. Therefore, our aim was to investigate the diagnostic value of four urinary biomarkers: human brain derived neurotrophic factor (hBDNF), malondialdehyde (MDA), h nerve growth factor (hNGF) and h 8‐hydroxydeoxyguanosine in women with OAB. These are neurotrophins/oxidative stress markers that have been linked to lower urinary tract symptoms. Methods: A total of 105 women were included in the study and distributed in two groups: a group with OAB (n = 53) and a control group (n = 50). The levels of the biomarkers were determined using enzyme‐linked immunosorbent assay technique and they were compared between the groups. If the Mann‐Whitney test demonstrated a statistically significant difference, receiver operating curves (ROC) analysis was undertaken. Results: When normalized to urinary creatinine, hBDNF, MDA, and hNGF showed significantly increased values in women with OAB as compared to controls, whereas 8‐OHdG showed no significant difference. The diagnostic performance of these biomarkers was analyzed based on the area under the ROC curve (AUC). MDA had the highest AUC (0.75), followed by hNGF (0.69) and hBDNF (0.67). Conclusions: Our findings suggest that MDA, a relatively novel biomarker in OAB research, has a fair performance as a diagnostic tool for OAB. Moreover, urinary neurotrophins (NGF and BDNF) as biomarkers may have a role in the diagnostic pathways of women with OAB symptoms. [ABSTRACT FROM AUTHOR]

Objective: To investigate the relationships of levels of serum 8-hydroxydeoxyguanosine ( 8 -OHDG) and vertebral protein like protein 1 ( VILIP-1 ) with the pathological characteristics and prognosis of patients with cerebral hemorrhage. Methods: Totally 118 patients with cerebral hemorrhage ( cerebral hemorrhage group ) and 100 healthy volunteers ( control group) were selected. Serum levels of 8 -OHDG and VILIP-1 were detected, and the relationships between the serum 8-OHDG and VILIP-1 levels and the pathological characteristics and prognosis of patients with cerebral hemorrhage were analyzed. Results: The levels of serum 8-OHDG and VILIP-1 in the cerebral hemorrhage group were higher than those in the control group (P < 0. 05 ). The levels of serum 8-OHDG and VILIP-1 in patients with massive hemorrhage, severe cerebral hemorrhage and poor prognosis were higher than those in patients with moderate hemorrhage and moderate cerebral hemorrhage and good prognosis ( both P < 0. 05 ). Serum levels of 8 -OHDG and VILIP-1 in patients with moderate hemorrhage, moderate cerebral hemorrhage were higher than those in patients with minor hemorrhage and mild cerebral hemorrhage ( both P < 0. 05 ). Pearson correlation analysis showed that serum 8-OHDG and VILIP-1 levels were positively correlated with cerebral hemorrhage and Scandinavian stroke scale ( SSS ) score (r = 0. 462, 0. 421, 0. 436, 0. 426, all P < 0. 05 ), and negatively correlated with Glasgow outcome ( GOS ) (r = - 0. 519, - 0. 504, all P < 0. 05 ) The area under the ROC curve ( AUC ) of serum 8-OHDG, VILIP-1, and 8 -OHDG + VILIP-1 was 0. 822, 0. 696, and 0. 943, respectively, the sensitivities were 84. 21 %, 71. 93%, 92. 98%, and specificities were 81. 97%, 70. 79%, and 95. 08%, respectively. Conclusion: Serum 8-OHDG and VILIP-1 levels increase significantly in patients with cerebral hemorrhage, and are related to the cerebral hemorrhage amount, the neurological impairment degree and the prognosis, which can be used as auxiliary indexes to evaluate the prognosis of patients with cerebral hemorrhage. [ABSTRACT FROM AUTHOR]

Background: Oral submucous fibrosis (OSMF) is one of the common potentially malignant disorders prevailing in India. The primary etiological factors include tobacco and arecanut, which contain numerous reactive oxygen species (ROS). ROS attack guanine bases in DNA and form 8-hydroxydeoxyguanosine (8-OHdG), which can be detected in patients who have diseases associated with oxidative stress. The oxidative DNA damage produced by oxidative stress may induce malignant transformation. Aim: The aim of the present study is to detect the expression of 8-OHdG in OSMF patients and compare the expression within different grades of OSMF and also normal buccal mucosa. Materials and Methods: A total of 30 samples were examined for the immunohistochemical expression of 8-OHdG. The control group included 10 formalin-fixed paraffin-embedded tissue blocks of the normal buccal mucosa. The study group includes 20 cases of formalin-fixed paraffin-embedded tissue blocks of OSMF (5 cases in each grade of very early, early, moderately advanced and advanced cases of OSMF). Three-micron thick tissue sections were made from each sample and stained with 8-OHdG antibody. The results were statistically analyzed using Kruskal–Wallis and Mann–Whitney U test Results: Statistically significant difference exists in the intensity of 8-OHdG expression between the study groups. The P-value obtained was <0.001, which was highly statistically significant. Conclusion: The present study is the first attempt to evaluate the expression of 8-OHdG in tissue samples of OSMF that revealed the role of free radicals and oxidative DNA damage in these patients. Further research with larger sample size, clinicopathologic correlation and long-term follow-up will shed more light on the pathogenesis of OSMF. It will also be useful for the development of new therapeutic strategies targeting treatment modalities for OSMF. [ABSTRACT FROM AUTHOR]

Background and Aim: Exogenous 8‐hydroxydeoxyguanosine (8‐OHdG) was suggested as an inhibitor of Rac1 and NADPH oxidase (NOX). The aim of this study was to evaluate the effects of the exogenous 8‐OHdG on hepatic fibrogenesis in vitro and in vivo model of liver fibrosis. Methods: Adult Sprague–Dawley rats were allocated to sham‐operated rats (n = 7), rats that underwent bile duct ligation (BDL) (n = 6), and BDL rats treated with 8‐OHdG (60 mg/kg/day by gavage, n = 6). All rats were sacrificed on day 21. Double immunofluorescence staining between either NOX1 or NOX2 and α‐smooth muscle actin (SMA) in liver was performed. Hepatic fibrotic contents were assessed by hydroxyproline assay and quantified by Sirius red staining. In vitro, hepatic stellate cell (HSC) line LX‐2 and HHSteC cells were stimulated by angiotensin II (10 μM). The reactive oxygen species (ROS) production was measured by confocal microscopy. The expressions of NOX1, NOX2, α‐SMA, transforming growth factor (TGF)‐β1, and collagen Iα were analyzed by quantitative real‐time polymerase chain reaction or immunoblotting. Results: The 8‐OHdG treatment in BDL rats reduced the NOX1 and NOX2 protein expression, which overlapped with α‐SMA compared with BDL rats. The 8‐OHdG treatment in BDL rats significantly decreased the mRNA expression of NOX1, NOX2, α‐SMA, TGF‐β1, and collagen Iα, and fibrotic contents. Increases of ROS production, Rac1 activation, NOX1, NOX2, and fibronectin expression induced by angiotensin II in HSCs were attenuated by 8‐OHdG. Conclusions: Rac1 activation and NOX‐derived ROS are implicated to liver fibrosis. The 8‐OHdG ameliorates liver fibrosis through the inhibition of Rac1 activation and NOX‐derived ROS. [ABSTRACT FROM AUTHOR]

In this study, the effect of Morus nigra (M. nigra) on carbon tetrachloride (CCI4)-induced hepatic injury in the rat was investigated. A hepatotoxic rat model was developed by the injection of CCI4 dissolved in soybean oil (1 mL/kg/twice a week, intraperitoneal (i.p.) injection). Following the formation of hepatic injury, extracts of M. nigra at doses ranging from 150 to 300 mg/kg were administered to rats by i.p. injection for eight weeks. At the end of administration, rat livers were excised by dissection. The activities of liver enzymes, alanine aminotransferase (ALT), aspartate aminotransferase (AST) and gamma-glutamyl transferase (GGT) were detected in the serum, and the activities of antioxidant enzymes, superoxide dismutase (SOD) and glutathione peroxidase (GPx), were established in the liver. Histological changes and immunohistochemical localization of caspase-3 and 8-oxo-2’-deoxyguanosine (8-OhdG) were performed by hematoxylin-eosin (H&E) staining of liver sections and caspase-3 and 8-OhdG immunohistochemical staining. The results showed that the M. nigra extract prevented protein oxidation generated by CCI4. The extracts demonstrated the ability to modulate the activity of SOD and GPx, and also prevented the CCI4-induced increase in AST and GGT levels. These results indicate that M. nigra extracts provided significant protection against CCl4-induced hepatic injury and might also present a novel approach for the treatment of some liver diseases.

In this study, we evaluated the bystander effect of radiation on the regulation of cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), and 8-hydroxydeoxyguanosine (8-OHdG) in lung tissues of Sprague-Dawley rats with and without pre-administration of melatonin. A 2×2 cm2 area of the pelvis of male Sprague-Dawley rats with and without pre-administration of melatonin (100 mg/kg) by oral and intraperitoneal injection was irradiated with a 3 Gy dose of 1.25 MeV γ-rays. Alterations in the levels of COX-2, iNOS, and 8-OHdG in the out-of-field lung areas of the animals were detected by enzyme immunoassay. The bystander effect significantly increased COX-2, iNOS, and 8-OHdG levels in non-targeted lung tissues (P

Objective: Oxidative stress plays a key role in the pathogenesis of male infertility. But, the adverse effects of oxidative biomarkers on sperm quality remain unclear. This study aimed to investigate the levels of nitric oxide (NO), 8-hydroxydesoxyguanosine (8-OHdG), and total antioxidant capacity (TAC) oxidative biomarkers in seminal plasma and their relationship with sperm parameters. Methods: A total of 77 volunteers participated in the study, including fertile (n=40) and infertile men (n=37). NO, 8-OHdG, and TAC levels were measured using the ferric reducing ability of plasma, Griess reagent method and an enzyme-linked immunosorbent assay kit, respectively. Results: The mean values of sperm parameters in the infertile group were significantly lower than those in the fertile group (p<0.001). The mean 8-OHdG in the seminal plasma of infertile men was significantly higher (p=0.013) than those of controls, while the mean TAC was significantly lower (p=0.046). There was no significant difference in NO level between the two groups. The elevated seminal 8-OHdG levels were negatively correlated with semen volume, total sperm counts and morphology (p<0.001, p=0.001 and p=0.052, respectively). NO levels were negatively correlated with semen volume, total sperm counts and morphology (p=0.014, p=0.020 and p=0.060, respectively). Positive correlations between TAC and both sperm count and morphology (p=0.043 and p=0.025, respectively) were also found. Conclusion: These results suggested that increased levels of NO and 8-OHdG in seminal plasma could have a negative effect on sperm function by inducing damage to the sperm DNA hence their fertility potentials. Therefore, these biomarkers can be useful in the diagnosis and treatment of male infertility. [ABSTRACT FROM AUTHOR]

8-Hydroxydeoxyguanosine (8-OHdG) is one of the main products of DNA oxidative stress injury and has been widely used for quantitative analyzing ROS levels. However, the intracellular detection of 8-OHdG is rarely reported and could provide for a novel tool for oxidative damage research. Here, a highly fluorescent silver nanocluster was synthesized by conjugating 12 cytosine bases as Ag nanocluster templates with 8-OHdG aptamer as the specific binding target (named 8-OHdG-12C), resulting in a 10-fold increase in fluorescence intensity of the as-synthesized probe. The 8-OHdG-12C@AgNCs showed a good fluorescence property and were stable for weeks. In addition, it can visualize intracellular 8-OHdG in a spatiotemporal manner. We used oxidative or reductive inducers of ROS and showed that the probe was located within cells and proportional to the cell oxidative damage induced. Together, these results indicate that 8-OHdG-12C@AgNCs hold great potential for in vivo 8-OHdG detection and may be a useful method to determine how DNA oxidative damage influences cancer cells and apoptosis. [ABSTRACT FROM AUTHOR]

Environmental exposure to arsenic may be involved in the disturbance of DNA hypomethylation. The aim of this study is the first to explore the effect of interactions of urinary total arsenic levels, arsenic methylation capacity, 8-hydroxy-2′-deoxyguanosine (8-OHdG), plasma folate, and global 5-methyl-2′-deoxycytidine (5-MedC) levels on the risk of urothelial carcinoma (UC). A hospital-based case–control study was constructed. The research involved the histological recruitment and pathological verification of 178 UC patients and 356 age-/sex-matched controls without prior history of cancer. Arsenic species were determined by high-performance liquid chromatography (HPLC)—hydride generation and atomic absorption. 5-MedC levels were detected by HPLC and triple-quadrupole mass spectrometry (MS). 8-OHdG was processed by an online solid-phase extraction LC–MS/MS. Plasma folate levels were measured using the chemiluminescent technology. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated by multiple logistic regression analysis. Results indicate that the high levels of total urinary arsenic, inorganic arsenic percentage, and 8-OHdG and the low levels of DMA % and plasma folate were independent factors of UC. In addition, global 5-MedC levels in the first quartile versus fifth quartile significantly increased the twofold OR of UC after potential factors were adjusted (95% CI:1.10–4.03). The interaction of 5-MedC level and high total arsenic level, insufficient arsenic capacity, high 8-OHdG, and low folate levels was insignificant. Results of stepwise logistic regression analysis indicate that high total urinary arsenic levels (Q3 versus Q1), low plasma folate level, and low global 5-MedC (Q4 versus Q5) significantly increased the ORs of UC. The above results suggest that high total arsenic, low plasma folate, and 5-MedC levels affect the ORs of UC independently. [ABSTRACT FROM AUTHOR]

A quantitative assessment of the genotoxicity of silver nanoparticles (AgNPs) ascribed to its transplacental transfer and tissue distribution in pregnant rats was carried out in this study. A single intravenous (i.v.) injection of AgNPs with a size range from 4.0 to 17.0 nm was administered to pregnant rats at a dose of 2 mg/kg b.w. on the 19th day of gestation. Five groups beside control, each of the five rats were euthanized after 10 min, 1, 6, 12, or 24 h, respectively. The accumulation of nanoparticles (NPs) in mother and fetal tissues was quantified by inductively coupled plasma optical emission spectroscopy, where the highest accumulation level was recorded in maternal blood (0.523 µg/ml) after 24 h of administration. AgNPs induced accumulation in spleen tissue higher than placenta and fetal tissue homogenates. The data showed significantly detected levels of 8-hydroxydeoxyguanosine in all collected samples from administered animals compared with untreated individuals. Level of 8-OHdG in amniotic fluid exhibited the greatest values followed by maternal spleen, kidneys, and liver, respectively. Investigation by transmission electron microscope showed that the transfer of AgNPs through placental wall caused indentation of nuclei, clumped chromatin, pyknotic nuclei, and focal necrotic areas, while AgNPs appeared mainly accumulated in the macrophages of the spleen. Therefore, the data assume that the genotoxicity studies of AgNPs must be recommended during a comprehensive assessment of the safety of novel types of NPs and nanomaterials. Additionally, exposure to AgNPs must be prevented or minimized during pregnancy or prenatal periods. [ABSTRACT FROM AUTHOR]

Periodontal disease is one of the most prevalent oral diseases affecting the supporting tissues of the teeth, gingiva, periodontal ligament, cementum, and alveolar bone. Periodontal diseases are inflammatory disorders; oxidative stress (OxS) plays an important role in the pathogenesis of periodontitis, which can cause damage to genetic biomolecules such as proteins, lipids, and DNA. Increased OxS leads to oxidative damage of DNA with the formation of 8-hydroxydeoxyguanosine (8-OHdG) which is excreted in body fluids including gingival crevicular fluid (GCF) and saliva. 8-OHdG is used as a standard biomarker of oxidative DNA damage mainly due to its reliable detectability [ABSTRACT FROM AUTHOR]

8-Hydroxydeoxyguanosine (8-OHdG) is well known not only as an effective biomarker of oxidative stress but also as a mutagenic DNA modification. Incorporation of dAMP at the opposite site of 8-OHdG induces G>T or A>C transversions. However, in vivo analyses of gene mutations caused by potassium bromate (KBrO 3), which can induce 8-OHdG at carcinogenic target sites, showed that G>T was prominent in the small intestines of mice, but not in the kidneys of rats. Because KBrO 3 was a much clearer carcinogen in the kidneys of rats, detailed analyses of gene mutations in the kidney DNA of rats treated with KBrO 3 could improve our understanding of oxidative stress-mediated carcinogenesis. In the current study, site-specific reporter gene mutation assays were performed in the kidneys of gpt delta rats treated with KBrO 3. Groups of 5 gpt delta rats were treated with KBrO 3 at concentrations of 0, 125, 250, or 500 ppm in the drinking water for 9 weeks. At necropsy, the kidneys were macroscopically divided into the cortex and medulla. 8-OHdG levels in DNA extracted from the cortex were dramatically elevated at concentrations of 250 ppm and higher compared with those from the medulla. Cortex-specific increases in mutant frequencies in gpt and red/gam genes were found at 500 ppm. Mutation spectrum and sequence analyses of their mutants demonstrated significant elevations in A>T transversions in the gpt gene and single base deletions at guanine or adenine in the gpt or red/gam genes. While A>T transversions and single base deletions of adenine may result from the oxidized modification of adenine, the contribution of 8-OHdG to gene mutations was limited despite possible participation of the 8-OHdG repair process in guanine deletion. • KBrO 3 increased 8-OHdG and mutant frequency specifically in the renal cortex of rats. • KBrO 3 induced A>T transversion and single bp deletion at G and A in the renal cortex. • KBrO 3 -induced gene mutation partially caused through repair process of 8-OHdG. • KBrO 3 induced 8-OHdG and gene mutations, but the contribution of 8-OHdG was limited. [ABSTRACT FROM AUTHOR]

Bronchopulmonary dysplasia (BPD) remains the most common complication of very low birth weight (VLBW) preterm infants, and inflammatory regulation plays a role in the development of the BPD. Interleukin-6 (IL-6) has an important role in airway inflammation and therefore can be used as a marker of airway injury. The study aimed to compare the changes between IL-6 and oxidative stress marker with 8-hydroxy-2′-deoxyguanosine (8-OHdG) from serum and tracheal aspiration (TA) in VLBW preterm infants following development of BPD. Methods: This birth cohort study enrolled 80 VLBW preterm infants, including 26 who developed BPD. All infants completed the study and survived at 36 weeks postmenstrual age. IL-6 and 8-OHdG concentrations from serum and TA on Day 1 and Day 28 after birth were measured using immunoassay. Results: IL-6 and 8-OHdG in serum and TA were higher in the BPD group than in the non-BPD group on the 1st day after birth (p

Abstract Objective Association of oxidative DNA damage with gain in anthropometric indices has not been fully elucidated. Methods In this study, participants (n = 1151) were derived from the baseline visit of Wuhan residents in the Wuhan-Zhuhai Cohort Study. The participants finished the physical examinations at both baseline and 3-year follow up. Urinary levels of 8-hydroxydeoxyguanosine (8-OHdG) were measured by gradient-elution high performance liquid chromatography method and then calibrated by urinary creatinine (Cr) values. Results Generalized linear models showed that after adjusted for confounding factors, baseline central obesity individuals with a ≥2.5% hip circumference (HC) loss or >5% HC gain had a 0.290 μmol/mol Cr (95% confidence interval (CI): 0.108, 0.472) or 0.553 μmol/mol Cr (95% CI: 0.273, 0.833) increase in urinary 8-OHdG levels compared with those with a −2.5%–2.5% HC gain (both P < 0.05). Moreover, compared with non-central obesity at both baseline and 3-year follow-up, we observed that central obese men at both baseline and 3-year follow-up had a 0.46 μmol/mol Cr (95% CI: 0.16, 0.75) increased in urinary 8-OHdG levels. Conclusions HC gain showed dose-dependent associations with urinary 8-OHdG levels. Moreover, male central obesity at both baseline and 3-year follow-up had an increased risk for urinary 8-OHdG levels. Highlights • Adults with ≥2.5% HC loss increased urinary 8-OHdG levels. • Baseline central obesity with >5% HC gain was at higher risk of increasing 8-OHdG. • Developed central obesity during the 3-year follow-up had higher urinary 8-OHdG. [ABSTRACT FROM AUTHOR]

This study explored the effects of long-term bathing in radon hot springs on oxidative damage and antioxidation function in humans. In this study, blood was collected from residents in the Pingshan radon hot spring area (RHSA), Jiangzha RHSA, and control area (CA). 8-Hydroxydeoxyguanosine (8-OHdG) and thioredoxin reductase (TrxR), representing oxidation and antioxidant levels, respectively, were analyzed as indices. Compared to the CA group, the RHSA group in the Pingshan and Jiangzha areas showed significantly decreased 8-OHdG levels (Z =-3.350, -3.316, respectively, P < .05) and increased TrxR levels (Z =2.394, 3.773, respectively, P < .05). The RHSA and CA groups in Jiangzha had lower levels of TrxR and 8-OHdG compared to those in Pingshan. This finding may be related to the different radon concentration levels, bathing time and other factors. Results suggested that long-term bathing in radon hot spring may activate antioxidant function and reduce oxidative damage in the body. [ABSTRACT FROM AUTHOR]

Objective: This study investigated the effects of high haem oxygenase-1 (HO-1) expression on oxidative injury and the biological behaviours of rat dermal fibroblasts, under high glucose conditions. Method: Rat dermal fibroblasts were cultured in normal glucose (1.0g/l), high glucose (4.5g/l) or haemin (5μm). A bilirubin kit, real-time polymerase chain reaction (RT-PCR) and Western blotting measured the protease activity, mRNA, and protein levels of HO-1, respectively. An enzyme-linked immunosorbent assay (ELISA) kit measured media levels of 8-hydroxydeoxyguanosine (8-OHdG), reactive oxygen species (ROS) and collagen (hydroxyproline) secretion. Cell proliferation was measured using flow cytometry. Cell apoptosis was measured using Hoechst 33258 staining and flow cytometry. The transwell method and scratch test evaluated cell migration. Results: HO-1 expression exhibited a time-dependent change that was lowest in the high glucose (HG) group at 96 hours compared with the normal glucose (NG) group. In the HG group, the 8-OHdG, ROS and cell apoptosis were increased, and collagen secretion, cell proliferation and cell migration (horizontal and vertical) were decreased compared with the NG group at 96 hours. Haemin treatment sustained high HO-1 expression for at least 96 hours, and the cells exhibited decreased 8-OHdG and ROS, increased collagen synthesis, improved proliferation and migration ability, and decreased apoptosis in the NG and haemin (NH) group/HG and haemin (HH) group compared with the NG/HG groups. These cells recovered from oxidative injury and biological behaviours dysfunction. Conclusion: Haemin induces HO-1 expression in fibroblasts and it may influence the oxidative injury and biological behaviours of fibroblasts. These findings suggest that HO-1 may accelerate the healing of diabetic wounds via alleviation of oxidative injury and improvement of biological behaviours of fibroblasts. [ABSTRACT FROM AUTHOR]

Pelvic organ prolapse (POP) is a common and distressing health problem in adult women, but the pathophysiological mechanism is yet to be fully elucidated. Previous studies have indicated that oxidative stress may be associated with POP. Thus, the aim of the present study was to investigate the oxidative status of pelvic supportive tissue in POP and further demonstrate that oxidative stress is associated with the pathogenesis of POP. A total of 60 samples were collected from females undergoing hysterectomy for POP or cervical intraepithelial neoplasia (CIN). This included 16 females with POP II, 24 females with POP III-IV (according to the POP-Q system) and 20 females with CIN II-III as the control group. Immunohistochemistry was utilized to measure the expression of oxidative biomarkers, 8-hydroxydeoxyguanosine (8-OHdG) and 4-hydroxynonenal (4-HNE). Major antioxidative enzymes, mitochondrial superoxide dismutase (MnSOD) and glutathione peroxidase 1 (GPx1) were measured through reverse transcription-quantitative polymerase chain reaction, western blotting and enzyme activity assays. The results demonstrated that in the cardinal ligament, the expression of 8-OHdG and 4-HNE was higher in the POP III-IV group compared with the POP II group and control group. The MnSOD and GPx1 protein level and enzyme activity were lower in the POP III-IV group compared with the POP II or the control group, while the mRNA expression level of MnSOD and GPx1 was increased. In conclusion, oxidative damage is increased in the pelvic supportive ligament of female patients with POP and the antioxidative defense capacity is decreased. These results support previous findings that oxidative stress is involved in the pathogenesis of POP. [ABSTRACT FROM AUTHOR]

Background: Familial Mediterranean fever (FMF) is an inherent autoinflammatory disease and have a high prevalence in Mediterranean countries. The aim of this study was to evaluate salivary levels of oxidative stress parameters in patients with FMF and chronic periodontitis.Methods: The study population consists of 81 patients with FMF and 85 systemically healthy controls. The test and control groups were classified as chronic periodontitis and periodontally healthy [FMF-periodontitis (n = 37); FMF-periodontally healthy (n = 44); systemically healthy-periodontitis (n = 37); systemically and periodontally healthy (n = 48]. Total salivary samples were collected. Clinical periodontal parameters including plaque index, gingival index (GI), probing depth (PD), the percentage of bleeding on probing (BOP%), and clinical attachment level (CAL), were measured. Salivary total antioxidant status (TAS), total oxidant status (TOS), 8-hydroxydeoxyguanosine (8-OHdG), malondialdehyde (MDA), and oxidative stress index (OSI) were evaluated.Results: The FMF-periodontitis group had significantly higher levels of 8-OHdG, MDA, and OSI than that of the FMF-periodontally healthy group. In the FMF-periodontitis group, PD, 8-OHdG, MDA, and OSI levels were significantly higher than in the systemically healthy-periodontitis group (P = 0.035, P = 0.000, P = 0.000, and P = 0.000, respectively). 8-OHdG values were significantly correlated with BOP% and GI, and TOS values were significantly correlated with PD and CAL in the FMF-periodontitis group.Conclusions: In the presence of FMF and chronic periodontitis, there were increased salivary levels of oxidative stress. Thus, oxidative stress could be an important inflammatory mechanism in the FMF and chronic periodontitis. Further studies need to clarify the oxidative mechanisms of FMF and chronic periodontitis. [ABSTRACT FROM AUTHOR]

Background and Objectives: Oxidative stress is a common mediator in pathogenicity of established cardiovascular risk factors. The purpose of this study was to determine effects of selected aerobic training on some oxidative stress indicators in sedentary elderly women. Methods: In this quasi-experimental study, 21 participants (age range: 60-70 years) were selected by convenience sampling and then randomly assigned to an exercise group (n=11) and a control group (n=10). Aerobic exercise was performed at 50-70% of heart rate reserve for 45-60 minutes per session, three sessions a week, for eight weeks. Blood samples were taken at baseline and 24 hours after the last training session. Within-group and between-group differences were assessed using paired sample t-test and independent t-test, respectively. Statistical significance level was set at 0.05. Results: Weight, body mass index and body fat percentage decreased significantly after the exercise intervention (P<0.05). We also noted a significant reduction in endothelin- 1 levels in both groups (P<0.05). Nitric oxide increased significantly after the eight-week exercise training (P<0.05). Moreover, serum 8-hydroxydeoxyguanosine levels decreased significantly in the exercise group (P<0.05). No significant change was observed in malondialdehyde and urinary 8-hydroxydeoxyguanosine levels in both groups. The result also showed a significant difference in subjects' weight and in nitric oxide and 8- hydroxydeoxyguanosine levels between the two groups (P<0.05). Conclusion: It seems that regular aerobic exercise at moderate intensity can improve antioxidative capacity and reduce the risk of cardiovascular disease in elderly women. [ABSTRACT FROM AUTHOR]