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랫드간장상피세포에서 카드뮴에 의한 산화적 스트레스 및 Cytoskeleton 손상 유발에 관한 연구
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  • 랫드간장상피세포에서 카드뮴에 의한 산화적 스트레스 및 Cytoskeleton 손상 유발에 관한 연구
저자명
정상희,조명행,조준형
간행물명
Journal of toxicology and public health : an official journal of the Korean Society of Toxicology
권/호정보
1998년|14권 4호|pp.577-585 (9 pages)
발행정보
한국독성학회
파일정보
정기간행물|
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이 논문은 한국과학기술정보연구원과 논문 연계를 통해 무료로 제공되는 원문입니다.
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기타언어초록

Cadmium is an important industrial and environmental pollutant and has adverse effects on cell growth and metabolism, although the mechanisms of its cellular toxicity are still unclear. This study was performed to elucidate the cytotoxic mechanism of cadmium in the viewpoint of oxidative stress and cytoskeleton alterations in WB-F344 rat liver epithelial cells. 200 $mu extrm{M}$ $CdCl_2$ caused a severe disassembling of microtubule and micro filament and an apparent cell retraction under an observation with fluorescence micoscope. (equation omitted)-tubulin and F-actin protein were highly thiolated at 20 min and then disappeared from 1 hour after the treatment of 200 $mu$M CdCl$_2$in the immunoblot analysis. Intracellular GSH was decreased from 1hr to 24 hrs by 66.6 or 200 $mu extrm{M}$ of $CdCl_2$. Intracellular protein thiol was also decreased by 22.2, 66.6 and 200 $mu extrm{M}$ of $CdCl_2$ at 1 hour after its treatment. The product of lipid peroxidation (malondialdehyde) was increased from 4 hrs by 66.6 and 200$mu extrm{M}$ of $CdCl_2$. These data indicate that cadmium induces oxidative stress involving disassembling of microtubule and micro filament, thiolation of (equation omitted)-tubulin and actin protein, depletion of GSH and protein thiol, and increase of lipid peroxidation.