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Nicotine 및 Tobacco-Specific Nitrosamine이 발암과정에 미치는 영향
강호일(Hoil Kang),박미선(Mi Sun Park),김옥희(Ok Hee Kim) 한국환경성돌연변이발암원학회 2005 한국환경성돌연변이·발암원학회지 Vol.25 No.3
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 ㎎/㎏) 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 μmol/㎏) and sodium nitrite (180 μmol/㎏), nicotine, sodium nitrite and NNK (120 nmol/㎏) 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.
사람 백혈구 및 위 조직중의 8-Hydroxy-2'-Deoxyguanosine 측정에 관한 연구
강호일(Hoil Kang),엄미옥(Mi Ok Eom),박미선(Misun Park),염태경(Tai Kyung Ryeom),지승완(Seung Wan Jee),전해명(Hea Myung Jeon),김옥희(Ok Hee Kim) 한국환경성돌연변이발암원학회 2005 한국환경성돌연변이·발암원학회지 Vol.25 No.1
In the present study, we have measured 8-hydroxy-2'-deoxyguanosine in DNA of stomach cancers, adjacent stomach cancer tissues, normal stomach tissues and peripheral blood leukocytes of the same stomach cancer patients (n=48) to investigate their etiological association with gastric cancer and possibility whether peripheral blood leukocytes can use surrogate marker for early stomach cancer diagnosis by HPLC/ECD system. In normal stomach tissues, we found that 8-hydroxy-2'-deoxyguanosine levels in tissues infected with Helicobacter pylori were 1.4 fold higher than those in tissues without infected with Helicobacter pylori. However, in adjacent stomach cancer tissues, we found that 8-hydroxy-2'-deoxyguanosine levels in tissues infected with Helicobacter pylori were 1.5 fold lower than those in tissues without infected with Helicobacter pylori. In stomach cancer tissues, 8-hydroxy-2'-deoxyguanosine levels in tissues infected with Helicobacter pylori were not significantly different from those in tissues without infected with Helicobacter pylori. In Helicobacter pylori-negative specimens, 8-hydroxy-2'-deoxyguanosine levels of adjacent stomach cancer tissues were found to be significantly higher than those of normal stomach and cancer tissues. The 8-hydroxy-2'-deoxygnanosine levels of female were 1.7 fold higher than those of male in peripheral blood leukocytes of the same stomach cancer patients. The 8-hydroxy-2'-deoxyguanosine levels in Helicobacter pylori-negative specimens among adjacent stomach cancer tissues were found to be reversely correlated with those in peripheral blood leukocytes, suggesting that 8-hydroxy-2'-deoxyguanosine in peripheral blood leukocytes may not use as surrogate marker for the early diagnosis of human stomach cancer.
마우스피부암 발생과정에 있어서 텔로머레이저 활성에 관한 연구
강호일(Hoil Kang),지승완(Sung Wan Jee),김옥희(Ok Hee Kim) 한국환경성돌연변이발암원학회 2005 한국환경성돌연변이·발암원학회지 Vol.25 No.2
Telomerase, a specialized RNA-directed DNA polymerase that extends telomeres of eukaryotic chromosomes, has activity in most malignant tumors and provides a mechanism for the unlimited potential for division of neoplastic cells. Although telomerase is known to be a regulated enzyme, the factors and mechanisms involved in telomerase regulation are not well understood. In the present study, we compared the effect of 12-O-tetradecanoyl-phorbol-13-acetate (TPA) and non-phorbol ester tumor promoters such as okadaic acid, anthralin and benzoyl peroxide on the expression of telomerase in the mouse skin carcinogenesis system, a well characterized model for studying pre-malignant and malignant progression. We found that most early papillomas harvested after 10 weeks of TPA promotion showed telomerase activity. Other papillomas harvested after 10 weeks of okadaic acid, anthralin and benzoyl peroxide promotion and after single treatment of DMBA only also showed telomerase activity, respectively. On the other hand, normal and all skins surrounded by papillomas harvested after 10 weeks of these promoters has no telomerase activity. Taken together these results, there appears to be no clear association between the level of telomerase activity and protein phosphorylation in mouse skin papillomas and telomerase may be useful as bio-markers in early detection of tumors.
Chemical Transformation of Human Keratinocytes by 2,3,7,8-Tetrachlorodibenxo-ρ-dioxin
Mi-Kyung Kang,Young-Sill Choi,Tai-Kyung Ryeom,Mi-Ok Eom,Mi-Sun Park,Seung-Wan Jee,Kang-Ryune Kim,Ok-Hee Kim,Hoil Kang 한국환경성돌연변이발암원학회 2006 한국환경성돌연변이·발암원학회지 Vol.26 No.3
2,3,7,8-Tetrachlorodibenzo-ρ-dioxin (TCDD) is a ubiquitous, persistent environmental contaminant and the most powerful carcinogen categorized by IARC. Although the mechanism of carcinogenesis by TCDD is poorly understood, several studies have shown that the skin is one of target organs for TCDD. In this study, we investigated the neoplastic transformation of human keratinocyte-derived cell line, HaCaT, by chemical transformation method using N-methyl-N'-nitro-N-nitorsoguanidine (MNNG) and TCDD. We found that subsequent exposure to TCDD for 3 weeks after initial exposure to MNNG markedly induced transformed cells. It was suggested that TCDD can act as a potent promoter in HaCaT cells. Furthermore, these transformed cells showed morphological alternations in soft agar and increased telomerase activity. Therefore, the TCDD treatment of HaCaT cells by initiated with MNNG could promote neoplastic transformation without stimulation by exogenous growth factors. As a result, TCDD had a strong potency as a promoter in nontumorigenic immortalized human epidermal keratinocytes.
사람의 정상 피부세포 및 폐세포의 발암에 미치는 2,3,7,8-tetrachlorodibenzo-ρ -dioxin의 영향
강미경(Mi Kyung Kang),염태경(Tai Kyung Ryeom),김강련(Kang Ryune Kim),김옥희(Ok Hee Kim),강호일(Hoil Kang) 한국환경성돌연변이발암원학회 2006 한국환경성돌연변이·발암원학회지 Vol.26 No.3
2,3,7,8-Tetrachlorodibenzo-ρ-dioxin (TCDD) displays high toxicity in animals and has been implicated in human carcinogenesis. Although TCDD is recognized as potent carcinogens, relatively little is known about their role in the tumor promotion and carcinogenesis. It is known that TCDD can increase of cancer risk from various types of tissue by a mechanism possibly involving the aryl hydrocarbon receptor (AhR) activation. In this study, effects of TCDD on cellular proliferation of normal human skin and lung fibroblasts, Detroit551 and WI38 cells were investigated. In addition, to enhance our understanding of TCDD-mediated carcinogenesis, we have investigated process in which expression of Erk1/2, cyclinD1, oncogene such as Ha-ras and c-myc, and their cognate signaling pathway. TCDD that are potent activators of AhR-mediated activity was found to induce significant increase of cytochrome P4501A1 mRNA expression, suggesting a presence of functional AhR. These results support that CYP1A1 enzyme may be involved in the generation of TCDD-induced toxicity. Moreover mitogen-activated protein kinases (MAPKs) phosphorylation and cyclin D1 overexpression are induced by TCDD, which corresponded with the progression of cellular proliferation. However, TCDD did not affected Haras and c-myc mRNA expression. Taken together, it seems that TCDD are could be a part of cellular proliferation in non-tumorigenic normal human cells such as Detroit551 and WI38 cells through the upregulation of MAPKs signaling pathway regulating growth of cell population. Therefore, AhR-activating TCDD could potentially contribute to tumor promotion and Detroit551 and WI38 cells have been used as a detection system of tumorigenic effects of TCDD.
에스트로겐 수용체를 통한 카드뮴 독성 및 항산화제에 의한 독성경감에 관한 연구
김태성(Tae Sung Kim),강태석(Tae Seok Kang),강호일(Hoil Kang),문현주(Hyun Ju Moon),강일현(Il Hyun Kang),이영주(Young Joo Lee),최은희(Eun Hee Choi),홍진태(Jin Tae Hong),한순영(Soon Young Han),홍진환(Jin Hwan Hong) 한국환경성돌연변이발암원학회 2006 한국환경성돌연변이·발암원학회지 Vol.26 No.1
Cadmium, a human carcinogen, can induce toxicity in various cell lines and organs. Despite extensive research, the mechanisms of cadmium-induced cell toxicity and estrogenic potential in human are not clear. This study was performed to investigate cadmium-induced toxicity on human breast cancer cells :MCF-7 cells, an estrogen receptor (ER) positive breast cancer cells, and MDA-MB-231 cells, an ER negative breast cancer cells. MCF-7 cells was proved to be more sensitive than the other cell lines (IC50 = 50 μM at MCF-7 cells and 120 μM at MDA-MB-231). The expression of JNK and AP-1 transcription factors such as c-Jun and c-Fos dependent transcription were increased by cadmium treatment. Inhibition of ER activation by ER antagonist (tamoxifen or ICI 182,780) significantly recovered the viablity and inhibited apoptotic cell death. This suggested that cadmium-induced cell death in ER (+) cells was mediated by JNK/AP-1 pathway and this pathway was more stimulated by ER activated by cadmium. Co-treatment of antioxidants such as selenium (Se), butylated hydroxyanisole (BHA), glutathione (GSH), or N-acetyl-L-cysteine (NAC) recovered the cadmium-induced cell death in MCF-7 cells. Cadmium-induced lipid peroxidation was decreased by GSH, NAC, or BHA in MCF-7 cells. The expression of SOD protein was decreased by cadmium (100 μM) but recovered by GSH, NAC, BHA, or Se. Our data showed that the cadmium-induced cell toxicity in human breast cancer cells could be protected by the antioxidants (Se, BHA, NAC, GSH, or NAC) and ER antagonist (tamoxifen or ICI 182,780). Therefore, toxicity of cadmium in breast cancer were mediated by oxidative stress and ERα.
박호일(Hoil Park),서주봉(Jubong Seo),홍성유(Sungyou Hong),강수영(Suyoung Kang),김장균(Janggyeun Kim) 한국자동차공학회 2011 한국자동차공학회 부문종합 학술대회 Vol.2011 No.5
A flow noise radiating from a compressor housing of a vehicle turbocharge was investigated. The noise was induced by a vortex around the intake area of the compressor wheels - a intake flow noise, realized to be largely affected by a combination of the shape of the compressor scroll and that of compressor wheels by tests. And, its frequency did not increase proportionally to the turbocharger speed, and was located around the range of 1.6㎑ and 1.8㎑ to the whole working area of the turbocharger. Some countermeasures were tried to reduce the noise - helmholtz resonators, the change of the diffuser, the smaller compressor scroll, and a groove around the intake area of the compressor wheels. The smaller compressor scroll could effectively reduced the noise, but was not adopted because of the deterioration of the compressor performance. For the noise reduction, the groove was chosen because it could sufficiently reduce the noise and maintain the performance.