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스테로이드 합성을 교란하는 내분비계장애물질 검색을 위한 라이디히 세포 분리 및 배양조건 확립
강일현(Il Hyun Kang),강태석(Tae Seok Kang),강호일(Ho Il Kang),문현주(Hyun Ju Moon),김태성(Tae Sung Kim),기호연(Ho Hyun Ki),류혜원(Hye Won Ryu),신재호,동미숙(Mi Sook Dong),한순영(Soon Young Han),김승희(Seung Hee Kim),홍진환(Jin Hwan Hong 한국환경성돌연변이발암원학회 2006 한국환경성돌연변이·발암원학회지 Vol.26 No.2
Normally, environmental toxicants are classified as endocrine disruptors if they interfere with regulation of cellular function by endogeneous steroids through inhibition of receptor binding and/or transcriptional activation. So, many studies have been performed about agonist/antagonist of hormone receptor to study mechanisms of endocrine disruptors. If toxicants affect steroid biosynthesis and/or degradation and alter hormone homeostasis, these also are classified as endocrine disruptors. But there are not many studies of the mechanisms of endocrine disruptors on the basis of alteration of steroid biosynthesis and/or degradation. Isolation and culture of Leydig cells from testis is one of methods for the steroidogenesis screening assays to evaluate a substance for altering steroidogenesis. Leydig cells were harvested using the method described by Klinefelter with modifications. Leydig cells were purified by perfusion of testis and incubation (34℃, 80cycles/minute, 20 minutes) with collagenase (0.25 ㎎/㎏), centrifugal elutriation, percoll gradient centrifugation and BSA multidensity gradient centrifugation. To confirm if this method is one of appropriate tools to evaluate a substance for altering steroidogenesis, ketoconazole, positive control was administered to purified Leydig cells. Ketoconazole (10??M and above) significantly reduced testosterone production in purified Leydig cells. From above results, we suggest that this method for steroidogenesis screening assay appears to be a appropriate tool to detect suspected compounds for altering steroidogenesis.
LC-MS/MS를 이용한 인체시료 중 프탈레이트 대사체 동시분석법 확립
홍순근,남혜선,정기경,강일현,김태성,조상은,정수희,이장우,김준철,고영림,강태석,Hong, Soon-Keun,Nam, Hye-Seon,Jung, Ki-Kyung,Kang, Il-Hyun,Kim, Tae-Sung,Cho, Sang-Eun,Jung, Su-Hee,Lee, Jang-Woo,Kim, Jun-Cheol,Kho, Young-Lim,Kang, Tae-Se 한국환경보건학회 2010 한국환경보건학회지 Vol.36 No.6
Phthalates, such as di (2-ethylhexyl) phthalate (DEHP), dibutyl phthalate (DBP) have been proved to be teratogenics and endocrine disruptors, metabolized rapidly and excreted in the urine. In this study, a simultaneous analytical method for 10 phthalate metabolites, MnBP, MiBP, MBzP, MCHP, MEHP, MEHHP, MEOHP, MnOP, MiNP and MiDP, in human urines, based on switching system with on-line pretreatment column using HPLC-MS/MS has been developed. This method was validated according to the guideline of bioanalytical method validation of National Institute of Toxicological Research. Limits of detection range between 0.2 and 0.9 ng/ml for 10 phthalate metabolites. The calibration curves showed linearity in the range 0.997~0.999, and the results of the intra- and inter-day validations were in the range from 0.4 to 14.7% RSD and from 0.3 to 9.4% RSD, respectively. Recoveries of phthalate metabolites varied from 87.0 to 116.1%. This analytical method showed high accuracy and stable precision for all metabolites, and seems to be suitable for biomonitoring of phthalates in human urine.
항안드로겐성 물질이 성 성숙 이전 단계의 정소에서 미치는 영향 연구
홍진,한순영,문현주,강태석,강일현,김태성,김승희,권기성,Hong Jin,Han Soon-Young,Moon Hyun-Ju,Kang Tae-Seok,Kang Il-Hyun,Kim Tae-Sung,Kim Seung-Hee,Kwon Ki-Sung 환경독성보건학회 2006 환경독성보건학회지 Vol.21 No.3
The experiments investigated whether early exposure to testosterone propionate (TP) during prepuberty alters testis development in Sprague-Dawley male rats. We performed Hershberger assay using the stimulated weanling male rats by OECD protocols, cDNA microarray, and Western blot. TP was subcutaneously injected to uncastrated Sprague-Dawley male rat of 22 days old for 10 consecutive days at doses of 0.4, 0.8, 1.0, 1.2, 1.6 mg/kg per day. At necropsy, the following tissues were removed and weighed: combined testes, epididymides (Epi), Cowper's glands (COW), levator am, and bulbocavernosus muscles (LABC), seminal vesicles, together with coagulating gland (SV) and ventral prostate (VP). We found that TP increased the weights of Epi, VP, SV, COW, and LABC, while testis was decreased in a dose-dependent manner. In cDNA microarray analysis of testis, there were significant reductions in the expression of cytochrome P450 11A (CYP11A), the rate-limiting enzyme of steroidogenesis. Taken together these results, TP exposure before puberty in male rats may produce the delay in testis development by inhibiting the CYP11A gene expression.
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.
Cadmium Induces Apoptosis Through Oxidative Stress in Human Breast Cancer MCF-7 Cells
오지영,이수정,신재호,김태성,문현주,강일현,강태석,김안근,한순영,Oh Jy Young,Lee Su Jung,Shin Jae-Ho,Kim Tae Sung,Moon Hyun Ju,Kang Il Hyun,Kang Tae Seok,Kim An Keun,Han Soon Young The Korean Society of Environmental Toxicology 2004 환경독성보건학회지 Vol.19 No.3
본 연구는 건전지나 플라스틱 등 산업물질, 식품, 흡연 그리고 공기, 물 등을 통해 인간과 생태계에 노출되고 있는 중금속 카드뮴을 인간 유방암 세포 MCF-7에 처리하였을 때 일어나는 현상을 살펴보고 나아가 카드뮴의 독성기전을 규명하기 위해 시행되었다. 카드뮴으로 인한 아폽토시스는 DNA분절 현상과 핵의 쪼개짐, 세포주기에 있어서 sub-G1의 출현 그리고 아폼토시스시에 발현되는 단백질 caspase의 발현, 특히 산화적 스트레스상태에서 마이토콘드리아가 손상을 입었을 때 발현되는 caspase-9의 발현을 통해 확인하였다. 카드뮴으로 인한 산화적 스트레스는 활성 산소종이 대조군에 비해 증가하고 이를 방어하기 위한 항산화효소 superofide dismutase, catalase, glutathion redurtase가 감소함을 통하여 확인하였다. 이 상의 결과들을 통해 카드뮴은 인간 유방암 세포 MCF-7에서 산화적 스트레스를 유발시켜 아폼토시스를 일으키는 것으로 추정할 수 있다.