• 대한예방의학회:학술대회논문집
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• 1998.10b
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• pp.289-290
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• 1998

• Journal of Photoscience
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• v.9 no.2
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• pp.142-145
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• 2002

A strict anaerobe, Prevotella melaninogenica is highly sensitive to oxidative stress. Oxidative stress such as exposure to oxygen or addition of hydrogen peroxide, increased 8-hydroxydeoxyguanosine (80HdG), a typical of oxidative DNA damage, and decreased the bacterial cell survival rate. We could detect the generation of reactive oxygen species in P. melaninogenica after exposure to oxygen. UVA irradiation also increased 80HdG in the bacterium. On the other hand, such oxidative stress did not increase 80HdG in a facultative anaerobe. These findings suggest that P. melaninogenica is a suitable material to study the biological effects of oxidative stress, to evaluate antioxidants, and to study the effects of oxygen or reactive oxygen species on molecular evolution.

• 대한예방의학회:학술대회논문집
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• 1995.10a
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• pp.293-294
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• 1995

• 대한예방의학회:학술대회논문집
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• 2002.10a
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• pp.216-217
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• 2002

• Toxicological Research
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• v.8 no.2
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• pp.171-177
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• 1992

To investigate a short term screening method for carcinogenic quinone compounds, 8-hydroxydeoxyguanosine (8-OHdG), an oxidative DNA damage, was determined in the kidney and liver DNA isolated from Sprague-Dawley rats after i.p.injection of 7 mg/kg adriamycin (AM), 7mg/kg tetrahydropyranyladriamycin (THP), and 10mg/kg daunomycin (DM) by HPLC-electrochemical detector system. 8-OHdG was also determined from rat hepatocvtes and calf thymus DNA exposed to AM, DM and THP. When rats were treated with DM and THP, 8-OHdG was significantly increased in the kidney compared to control group, and remained at high level (7.9~9.0, 8-OHdG/dG${\times}10^4$)at the end of experiments (48hr after treatment). 8-OHdG level in cultured hepatocyte exposed to AM, DM and THP was 1.5~2 fold higher than control at all time points. (1,2,3,4hr after treatment). From calf thymus DNA exposed to AM, DM and THP, 8-OHdG was 2.5 fold higher than of control. These results suggest that quantitation of 8-OHdG may provide a useful marker for identifying target organ in oxidative chemical carcinogenesis and for short term screening of free radical generating carcinogens.

• Journal of the Korean Society of Food Science and Nutrition
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• v.30 no.6
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• pp.1220-1226
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• 2001

This study was conducted to investigate the effect of water-soluble extract from roasted chicory on the lipid metabolism and oxidative stress in male Sprague-Dawley rats. The experimental groups were divided into three groups ; the normal group, the cholesterol group and the chicory group. Roasted chicory extract was supplemented at 5.0% (w/w) level in the cholesterol diet. Concentration of total cholesterol in serum was significantly higher in the cholesterol group than in the normal group, but this increase in the cholesterol group was significantly decreased by the cholesterol diet supplemented with chicory extract. Concentration of HDL-cholesterol in serum was significantly lower in the cholesterol group than in the normal group, but this decrease in the cholesterol group tended to increase in the chicory group. However, concentrations of triglyceride, phospholipid and nonesterified fatty acid in serum were not significantly different among the groups. Concentrations of triglyceride and cholesterol in liver were significantly higher in the cholesterol and chicory groups than in the normal group. Feces weight and the excretion of cholesterol and bile acid into feces were significantly higher in the chicory group than in other groups. Concentrations of thiobarbituric acid reactive substances (TBARS) in homogenates and microsomal fractions of liver were not significantly different among the groups. On the other hand, concentration of 8-hydroxydeoxyguanosine (8-OHdG) as an useful marker of oxidative stress in urine was lower in the chicory group than in other groups. Concentration of serum glucose was signnificantly lower in the cholesterol group than in the normal group, but that of the chicory group was significantly higher than in the normal group. These results demonstrated that dietary chicory extract exerted the decreasing effect of cholesterol level and oxidative stress in cholesteral-fed rats.

• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2003.10a
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• pp.187-187
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• 2003

• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2004.05a
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• pp.62-62
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• 2004

• Journal of Preventive Medicine and Public Health
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• v.28 no.2 s.50
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• pp.511-525
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• 1995

To elucidate some DNA adducts as a biological marker for workers of chromate pigment, the effects of chromium exposure on the formation of 8-hydroxydeoxyguanosine(8-OH-dG) and sister chromatid exchanges(SCEs) frequency in 38 workers of a pigment plant in Bucheon which utilized lead chromates, were examined. The chromium contents of venous blood and urine were measured as working environmental exposure level. The concentrations of 8-OH-dG in DNA isolated from lymphocytes were determined with high performance liquid chromatography and electrochemical detector and denoted as a molar ratio of 8-OH-dG to deoxyguanosine(dG). The SCEs frequency were analyzed in DNA isolated from lymphocytes. A significant correlation was found between creatinine adjusted urine chromium concentration and the molar ratio of 8-OH-dG to dG(r=0.47, p<0.01). After adjusting the current smoking habit, the correlation coefficient was increased(r=0.62, p<0.05). However, there was no significant correlation between the SCE frequency and chromium exposure. This significant results between molar ratio of 8-OH-dG to dG and chromium exposure are in good agreement with in vitro studies that support the importance of DNA adduct formation for the carcinogenic effect of chromium.

• Environmental Mutagens and Carcinogens
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• v.25 no.3
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• pp.118-123
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• 2005

Nicotine has been implicated as a potential factor in the pathogenesis of human lung cancer, however its mechanism of action in the development of lung cancer remains largely unknown. To explore the role of nicotine in the development of lung cancer, we first investigated the effects of nicotine on the expression of tumor associated genes by treating Sprague-Dawley rats with nicotine (10 mg/kg) by gavage once daily for 10 days. We determined the expression of proteins and mRNAs of the ras, raf, myc, jun, fos oncogenes and p53, Rb tumor suppressor genes by Western and Northern blotting, respectively. We did not detect any changes on the levels of proteins and mRNAs of these tumor associated genes in the lung of Sprague-Dawley rats from 3 days to 12 weeks after the last treatment of nicotine, indicating that nicotine appears to have no effect on expression of these oncogenes and tumor suppressor genes at an early stage in multistage chemical carcinogenesis. In a second experiment, we investigated the possibility that 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) could be formed endogenously by treating with nicotine and sodium nitrite. We treated groups of Fischer 344 rats with nicotine ($60{\mu}mol/kg$) and sodium nitrite ($180{\mu}mol/kg$), nicotine, sodium nitrite and NNK (120 nmol/kg) alone by gavage once daily for 7 days, respectively and determined the 8-hydroxydeoxyguanosine (8-OHdG), as an indicator of NNK formation, in the lungs of rats 24 hours and 48 hours after the last treatment by HPLC/ECD method. We detect increased level of 8-OHdG in the lungs of rats treated with NNK, but in the case of nicotine plus sodium nitrite, nicotine and sodium nitrite alone we could not detected any changes of 8-OHdG, respectively.