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논문 기본 정보

자료유형
학술저널
저자정보
저널정보
대한의생명과학회 대한의생명과학회지 대한의생명과학회지 제11권 제4호
발행연도
2005.12
수록면
441 - 446 (6page)

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The molecular mechanism of ischemia / reperfusion injury remains unclear, Reactive oxygen species (ROS) are implicated in cell death caused by ischemia/reperfusion in vivo or hypoxia in vitro. Poly (ADP-ribose) polymerase (PARP) activation has been reported to be involved in hydrogen peroxide-induced cell death in renal epithelial cells. This study was therefore undertaken to evaluate the role of PARP activation in chemical hypoxia in opossum kidney (OK) cells. Chemical hypoxia was induced by incubating cells with antimycin A, an inhibitor of mitochondrial electron transport. Exposure of OK cells to chemical hypoxia resulted in a time-dependent cell death. In OK cells subjected to chemical hypoxia, the generation of ROS was increased, and this increase was prevented by the H<sub>2</sub>O<sub>2</sub> scavenger catalase. Chemical hypoxia increased PARP activity and chemical hypoxia-induced cell death was prevented by the inhibitor of PARP activation 3-aminobenzamide. Catalase prevented OK cell death induced by chemical hypoxia. H<sub>2</sub>O<sub>2</sub> caused PARP activation and H<sub>2</sub>O<sub>2</sub>-induced cell death was prevented by 3-aminobenzamide. Taken together, these results indicate that chemical hypoxia-induced cell injury is mediated by PARP activation through H<sub>2</sub>O<sub>2</sub> generation in renal epithelial cells.

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영어초록
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

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UCI(KEPA) : I410-ECN-0101-2009-510-017356821