• Preventive Nutrition and Food Science
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• v.7 no.1
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• pp.67-71
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• 2002

Capsaicin (trans-8-methyl-N-vanillyl-6-nonenarnide), a major pungent component of hot pepper, is known to exert antioxidative properties. In this study, we investigated the protective effects of capsaicin against chemical carcinogen-induced oxidative damage in rats. Male Sprague Dawley rats weighting 230~250 g were treated with chemical carcinogens such as 2-nitropropane (2NP) or n-methyl-N'-nitro-N-nitrosoguanidine (MNNG) after (or before) the administration of capsaicin at doses of 0.5, 1,5 mg/kg. The level of lipid peroxidation in rat liver was estimated by measuring the amounts of thiobarbituric acid reactive substances. The degree of oxidative DNA damage was evacuated by measuring a DNA adduct, 8-hydroxydeoxyguanosine (8-OHdG), in urine. Antioxidative activities of capsaicin and its metabolites in vitro were determined by the measurement of DPPH (1,1-diphenyl-2-picrylhydrazyl), a radical quencher. Significant inhibition of 2-NP induced lipid peroxidation was observed in the liver of the rat when treated with capsaicin. MNNG-induced urinary excretion of 8-OHdG was decreased by capsaicin treatment. Capsaicin and its metabolites inhibited net only the formation of free radicals, but also lipid peroxidation in vitro. Our results show that capsaicin may function as a free radical scavenger against chemical carcinogen-induced oxidative cellular damage in vivo. The observed antioxidative activities of capsaicin may play an important role in the process of chemoprevention.

• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2002.05a
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• pp.84-84
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• 2002

• Proceedings of the Korean Society of Toxicology Conference
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• 2003.10b
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• pp.187-187
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• 2003

This study evaluated the potential usefulness of urinary 1-hydroxypyrene glucuronide (1-OHPG) and 8-hydroxy-deoxyguanosine (8-OHdG) as biomarkers of the Asian Dust event. Urine samples were collected from 224 subjects (112 children and 112 their mothers) from Seoul (n=60), Inchon (n=104) and Pohang (n=60) in South Korea. (omitted)

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.13
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• pp.5199-5203
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• 2015

Background: Helicobacter pylori (H.pylori) is associated with chronic gastritis, peptic ulcers, gastric adenocarcinomas and mucosa associated tissue lymphomas. Cytotoxin associated gene A (CagA) is one of the virulence factors of H.pylori. It is hypothesized that reactive oxygen species (ROS) play roles in H.pylori associated disease especially in development of gastric adenocarcinoma. Individuals infected with H.pylori bearing CagA produce more ROS than others. 8-hydroxydeoxyguanosine (8OHdG) is an in vitro marker of DNA damage and oxidative stress. The aim of this study was to investigate the relationship between 8OHdG level, H.pylori infection and CagA and alterations of serum 8OHdG level after H.pylori eradication. Materials and Methods: Patients admitted with dyspeptic complaints and upper gastrointestinal endoscopy were assessed. H.pylori was determined from histopathology of specimens. Serum 8OHdG levels of three groups (H.pylori negative, H. pylori positive CagA negative and H.pylori positive CagA positive) were compared. Patients with H.pylori infection received eradication therapy. Serum 8OHdG levels pretreatment and posttreatment were also compared. Results: In total, 129 patients (M/F, 57/72) were enrolled in the study. Serum 8OHdG level of H.pylori negative, H. pylori positive CagA negative and H.pylori positive CagA positive groups were significantly different ($5.77{\pm}1.35ng/ml$, $5.43{\pm}1.14ng/ml$ and $7.57{\pm}1.25ng/ml$ respectively, p=0.05). Furthermore, eradication therapy reduced serum 8OHdG level ($6.10{\pm}1.54ng/ml$ vs $5.55{\pm}1.23ng/ml$, p=0.05). Conclusions: Individuals infected with H.pylori bearing CagA strains have the highest serum 8OHdG level and eradication therapy decreases the serum 8OHdG level. To the best of our knowledge this is the first study that evaluated the effect of CagA virulence factor on serum 8OHdG level and the effect of eradication therapy on serum 8OHdG levels together. Eradication of CagA bearing H.pylori may prevent gastric adenocarcinoma by decreasing ROS. 8OHdG level may thus be a good marker for prevention from gastric adenocarcinoma.

• Proceedings of the Korean Society of Toxicology Conference
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• 2002.05a
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• pp.84-84
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• 2002

Abstract To study the status of oxidative DNA damage in Helicobacter pylori infection in more details, gene-specific oxidative DNA damage was investigated by examining oxidative DNA damage to individual genes. This was done by determining the loss of PCR product of a targeted gene before and after gastric mucosal DNA was treated with 8-hydroxyguanine glycosylase, which cleaves DNA at the 8-hydroxyguanine residues.(omitted)

• Clinical and Experimental Reproductive Medicine
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• v.47 no.1
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• pp.54-60
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• 2020

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.

• Proceedings of the Korean Journal of Food and Nutrition Conference
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• 2000.05a
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• pp.13-20
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• 2000

Melatonin, a chemical mediator produced in the mammalian pineal gland and several other organ, is a ubiquitously acting antioxidant. It has been shown to scavenge the hydroxyl radical (ㆍOH), singlet oxygen ($^1$O$_2$) and the peroxynitrite anion (ONOO-). In addition, melatonin reportedly stimulates a number of antioxidative enzymes including glutathione peroxidase, glutathione reductase and glucose-6-phosphate dehydrogenase. Antioxidative effect of melatonin in pharmacological and physiological level was investigated using hepatocarcinogen 2-nitropropane (2-NP) and pinealectornized (Px) rats, respectively. Lipid peroxidation (LPO) as indicated by malondialdehyde and 4-hydroxyalkenals and DNA damage as indicated by 8-hydroxydeoxyguanosine (8-OH-dG) induced by 2-NP were prevented by melatonin. The degree of LPO and DNA damage in Px rats were higher than those of intact old and young ones suggesting the removal of pineal gland resulted in higher accumulation of oxidative damage.

• Journal of Life Science
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• v.14 no.3
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• pp.406-410
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• 2004

Glyoxal or methylglyoxal was incubated with catalase in 0.24 M sodium phosphate buffer (pH 7.4) at 37$^{\circ}C$. Dicarbonyls modify and inactivate catalase. Plasmid DNA that is directly incubated with glycation propagators, glyoxal and methylglyoxal, showed different DNA mobility shift compared to nomal plasmid DNA. When plasmid DNA is added in Fenton reaction with glycated catalase, plasmid DNA was significantly strand broken and 8-hydroxydeoxyguanosine production was time dependently increased. These results suggest that glycation of antioxidant is synergistic effect to oxidative stress.

• BMB Reports
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• v.36 no.2
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• pp.190-195
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• 2003

The Vitamin E (VE) effect was examined on oxidative damage to DNA, lipids, and protein in mice that were fed various levels of lipid diets after total body irradiation (TBI) with X-rays at 2 Gy. No increase of 8-hydroxydeoxyguanosine (8OHdG) by TBI was observed in the +VE group; however, in the case of the -VE group, a significantly higher 8OHdG level was observed in the high-lipid group than in the low- or basal-lipid group. In the groups with TBI, the concentration of thiobarbituric reactive substances (TBARS) only significantly increased in the high-lipid (-VE) group. These changes in TBARS, due to TBI, were not detected in other groups. The contents of protein carbonyls only increased in the (-VE) group. The contents of protein carbonyls was significantly different between the (+VE) and the (-VE) groups, regardless of the lipid levels. The concentrations of GSH, vitamins C and E in the liver were lower, and the concentration of non-heme iron in the liver was higher in the high-lipid group than in the low- and basal-lipid groups. These concentrations in the high-lipid group were significantly different between the (+VE) and the (-VE) groups. These results strongly suggest that mice that are fed a high-lipid diet are susceptible to TBI-induced oxidative damage. Also, decreases in the GSH levels and an increase in the iron level are involved in the mechanism of this susceptibility.

• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2002.05a
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• pp.36-42
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• 2002

Diesel exhaust (DE) has been recognized as a noxious mutagen and/or carcinogen, because its components can form DNA adducts. Mechanisms governing the susceptibility to DE and the efficiency of such DNA adduct formation require clarification. The transcription factor Nrf2 is essential for inducible and/or constitutive expression of a group of detoxification and antioxidant enzymes, and we hypothesized that the nrf2 gene knockout mouse might serve as an excellent model system for analyzing DE toxicity. To address this hypothesis, lungs from nrf2(-/-) and nrf2(+/-) mice were examined for the production of xenobiotic-DNA adducts after exposure to DE (3 $mg/m^{3}$ suspended particulate matter) for 4 weeks. Whereas the relative adduct levels (RAL) were significantly increased in the lungs of both nrf2(+/-) and nrf2(-/-) mice upon exposure to DE, the increase of RAL in the lungs from nrf2(-/-) mice exposed to DE were approximately 2.3-fold higher than that of nrf2(+/-) mite exposed to DE. In contrail, cytochrome P4501Al mRNA levels in the nrf2(-/-)mouse lungs were similar to those in the nrf2(+/-) mouse lungs even after exposure to DE, suggesting that suppressed activity of phase II drug-metabolizing enzymes is important in giving ise to the increased level of DNA adducts in the Nrf2-null mutant mouse subjected to DE. Importantly, severe hyperplasia and accumulation of the oxidative DNA adduct 8-hydroxydeoxyguanosine were observed in the bronchial epidermis of nrf(-/-) mite following DE exposure. These results demonstrate the increased susceptibility of the nrf2 germ line mutant mouse to DE exposure and indicate the nrf2 gene knockout mouse nay represent a valuable model for the assessment of respiratory DE toxicity.