• 대한예방의학회:학술대회논문집
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• 대한예방의학회 1993년도 제45차 추계 학술대회 연제집
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• pp.217-218
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• 1993

• 한국독성학회:학술대회논문집
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• 한국독성학회 2002년도 Molecular and Cellular Response to Toxic Substances
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• pp.138-138
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• 2002

8-hydroxydeoxyguanosine (oh8dG) potently inhibits proliferation of KG-1, a human leukemia cell line in vitro, but little is known regarding to molecular mechanisms mediating this effect. Here we demonstrate that treatment of KG-1, deficient in 8-oxoguanine glycosylase (OGG1) activity, with oh8dG lead to G1 arrest associated with a dramatic decrease in the levels of cyclin D3 and cyclin-dependent kinase 4 (cdk4) and accompanied by an increase in the expression of p21.(omitted)

• 대한예방의학회:학술대회논문집
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• 대한예방의학회 2005년도 제57차 추계 학술대회 연제집
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• pp.386-386
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• 2005

• 한국환경성돌연변이발암원학회:학술대회논문집
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• 한국환경성돌연변이발암원학회 2002년도 Molecular and Cellular Response to Toxic Substances
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• pp.138-138
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• 2002

• 생명과학회지
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• 제18권8호
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• pp.1173-1176
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• 2008

본 연구에서는 ALDH2 knockout 마우스를 이용하여 에탄올을 경구 투여한 후 간조직 및 뇌조직, 그리고 폐조직에서의 8-hydroxydeoxyguanosine (8-OHdG) 농도를 측정하여 각 장기에서의 산화적 유전자 손상정도를 평가하고 ALDH2 효소활성과의 관련성을 파악하였다. 간조직의 8-OHdG 농도는 에탄올 투여에 의해서도 유의하게 증가하지만 ALDH2 효소의 결핍이 더욱 큰 영향을 주는 것으로 확인되었다. 또한, 뇌조직과 폐조직의 8-OHdG 농도도 에탄올에 의해 모두 유의하게 증가하는 것으로 나타났으며 폐조직에서의 8-OHdG 농도는 ALDH2 효소의 활성에 따라 유의하게 영향을 받는 것으로 나타났다. 본 연구에서 에탄올의 반복적인 투여는 간조직 뿐 아니라 뇌조직과 폐조직에서도 산화적 유전자 손상을 유발하는 것으로 확인되었으며, 적어도 에탄올에 의한 간조직과 폐조직에서의 산화적 유전자 손상은 ALDH2 활성이 결핍된 경우에 더욱 커지는 것으로 조사되었다. 본 연구의 결과는 ALDH2 효소가 결핍된 사람에서 각종 암발생 위험도가 크게 나타나는 이유를 규명하는데 매우 중요한 근거자료로 활용될 수 있을 것으로 기대된다.

• 생명과학회지
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• 제20권4호
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• pp.618-622
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• 2010

본 연구는 비소에 대한 만성노출이 의심되는 일부 폐금속광산 주변 지역 주민 중 여성들을 대상으로 요중 비소 농도와 산화적 유전자 손상지표인 요중 8-hydroxydeoxyguanosine (8-OHdG) 농도와의 관련성을 평가하기 위해 시행되었다. 충청북도에 위치한 두 폐금속광산 지역 주민 중 여성 165명을 대상으로 요중 비소농도와 요중 8-OHdG의 농도를 측정하고 SPSS 12.0 통계프로그램을 이용하여 분석하였다. 조사 대상자들의 요중 비소농도는 기하평균이 $5.65\;{\mu}g/g$ creatinine으로 나타났으며 요중 비소와 8-OHdG 농도와의 관련성 분석에서는 상관계수 0.399 (p<0.001)의 유의한 상관성을 보였다. 이러한 관련성은 비소노출 농도가 낮은 경우가 노출농도가 높은 경우에 비해 상대적으로 높은 것으로 나타났다. 본 연구의 결과는 요중 8-OHdG 농도가 저농도의 비소에 만성적으로 노출된 여성에서 산화적 유전자 손상을 평가하는 좋은 지표가 될 수 있음을 시사한다.

• 한국응용약물학회:학술대회논문집
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• 한국응용약물학회 1993년도 제2회 신약개발 연구발표회 초록집
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• pp.82-82
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• 1993

허혈-재관류손상 심근세포의 DNA에서 8-hydroxydeoxyguanosine (8-OHdG) 생성을 검토하였다. 흰쥐 적출심장의 Langendorff 관류 표본에서 대동맥 차단에 의한 60분 허혈후 산소가 포화된 Kredb-Henseleit용액으로 30분간 재관류 하므로서 허혈-재관류 손상을 유도하였다. 재관류 후 심근세포에서 DNA를 추출하고 HPLC(EC detector)를 이용하여 8-OHdG를 측정하였다. 실험결과 허혈-재관류 심근세포의 DNA에서 8-OHdG 함량이 증가하였으며 이는 $O_2$ 제거물질인 superoxide dismutase와 OH 제거물질인 mannitol에 의하여 방지되었다. Xanthine oxidase외 경쟁적 길항약인 allopurinol도 8-OHdG 생성을 억제하였으며 단백분해효소 억제제인 phenylsulfonylfluoride 그리고 관류액에서 칼슘의 제거 또한 허혈-재관류 심근 DNA의 생성을 방지하였다. 이상의 결과 허혈심근의 재관류시 8-OHdG 생성이 증가하며 이는 재관류 손상과 같은 산화성 심근손상을 평가하는 좋은 Index가 될 수 있을 것으로 여겨진다.

• Journal of Preventive Medicine and Public Health
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• 제32권1호
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• pp.101-107
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• 1999

Objectives. To determine the effects of exposure to hexavalent chromium, 93 male Sprague-Dawley rats were exposed to hexavalent chromium solution. Methods. Rats were divided into 4 groups and exposed to 0.1ml of 0 mM, 0.4 mM, 2.0 mM, and 10.0 mM potassium chromate in the first experiment, and to 0.1 ml of 0 mM, 20 mM, 40 mM, and 80 mM in the second for consecutive 3 days by tracheal instillation. Three and 10 rats were the controls for the first and the second experiments, respectively. Lung tissues were then removed to measure the 8-hydroxydeoxyguanosine (8-OH-dG) level using the HPLC-ECD method, superoxide dismutase (SOD) activity using the cytochrome C method, and 8-hydroxyguanine endonuclease activity using the oligonucleotide nicking assay. Results. The results showed no significant linear relationship between chromium exposure level and 8-OH-dG level or 8-hydroxyguanine endonuclease activity. In the first experiment, 8-OH-dG level and 8-hydroxyguanine endonuclease activity increased in 0.4 mM group, and then decreased in 2.0 mM and 10.0 mM groups. The correlation coefficients between 8-OH-dG level and 8-hydroxyguanine endonuclease activity was statistically significant (P<0.01), and total SOD activity was elevated by chromium exposure in a dose-dependent manner (P<0.05). In contrast, there was no significant dose-response pattern or correlation in the secod experiment. Conclusions. Based on the fact that there was no linear relationship between chromium dose and 8-OH-dG level or activity of the repair enzyme, it seems unlikely that 8-OH-dG formation is the major mechanism of chromium carcinogenesis.

• Journal of Preventive Medicine and Public Health
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• 제27권1호
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• pp.84-106
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• 1994

Hyperbaric oxygen (HBO) therapy for carbon monoxide (CO) poisoning eventually inducing the hypoxia-reoxygenation condition, may produce oxygen free radicals, which forms 8-hydroxydeoxyguanosine (8-OH-dG) by attacking C-8 position of deoxyguanosine (dG) in DNA. Effects of oxygen partial pressure or duration of HBO therapy with or without CO poisoning on the tissue 8-OH-dG formation were investigated. Male Sprague-Dawley rats were grouped and exposed to air (control group), 4000 ppm of CO for 10 to 30 minutes (CO only group), air for 30 minutes after 30 minute exposure to 4000 ppm of CO(CO-air exposure group), HBO after 30 minute exposure to 4000 ppm of CO(CO-HBO group), or HBO therapy fo. $10{\sim}120$ minutes(HBO only group). The 8-OH-4G concentrations in the brain and the lung tissues were measured with high performance liquid chromatography and electrochemical detector (ECD). Average concentrations of the 8-OH-dG of each group were statistically compared. In the brain tissues, 8-OH-dG concentrations of the CO only group, the CO-air exposure group, and the CO-HBO group did not significantly differ from those of the control group. Similar insignificance was also found between the CO-HBO group and the HBO only groups. No appreciable dose-response relationship was observed between the 8-OH-dG concentration and the oxygen partial pressure or the duration of HBO. However, the 8-OH-dG concentrations of the 30 minute CO only group were higher than those of the CO-air exposure group (p-value<0.05). In the lung tissues, there were no significant differences between the 8-OH-dG concentrations of the control group and those of the CO only group, the CO-air exposure group, and the CO-HBO group. However, mean 8-OH-dG concentration of the CO-air exposure group was significantly higher than that of the CO only group under the same CO exposure condition(p-value<0.05). With the duration of CO exposure, the 8-OH-dG concentrations of the lung tissues decreased significantly (p-value<0.05). The concentrations of 8-OH-dG in the lung tissues proportionally increased with the duration of HBO, but no such relation was observed with the oxygen partial pressure. These results suggest that the brain may be more resistant to oxygen free radicals as compared with the lungs, and that oxygen toxicity following HBO may be affected by factors other than oxygen free radicals.

• 대한의생명과학회지
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• 제11권2호
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• pp.143-152
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• 2005

To investigate the exposure effect of polycyclic aromatic hydrocarbons (PAHs), we analyzed the relationship between urinary 8-hydroxydeoxyguanosine (8-OHdG) concentration and PAHs exposure. The study population contained 44 workers in steel-pipe coating and paint manufacture industries. We measured airborne total PAHs as an external dose, urinary 1-hydroxypyrene (1-OHP) as an internal dose of PAHs exposure, and urinary 8-OHdG as an effective dose of oxidative DNA damage. There was significant correlation between the urinary concentration of l-OHP and the environmental concentration of PAHs, pyrene, urinary cotinine, AST, and GGT. The mean of urinary 8-OHdG was $17.07\pm1.706{\mu}g/g$ creatinine in workers exposed to airborne PAHs. There was significant correlation between the urinary concentration of 8-0HdG and the airborne concentration of PAHs. From the results of stepwise multiple regression analysis about 8-OHdG, significant independents was total PAHs. In this study, there were significant correlation between the urinary concentration of 8-OHdG and the airborne concentration of PAHs. The urinary 1-OHP was effective index as a biomarker of airborne PAHs in workplace. But it was influenced by non-occupational PAHs source, smoking and biomarkers of liver function test.