지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술대회자료
- 저자정보
- 발행연도
- 2004.11
- 수록면
- 53 - 60 (8page)
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The pro-apoptotic effect of phenethyl isothiocyanate (PEITC) and the role of glutathione (GSH) in sulforaphane (SFN)-induced antioxidant response element-dependent gene expression were investigated. The caspase-3 and caspase-9 activities were stimulated by PEITC. The release of cytochrome c was time- and dose- dependent. SP600125 suppressed apoptosis induced by PEITC. Similarly, this JNK inhibitor attenuated both cytochrome c release and caspase-3 activation induced by PEITC. SFN is converted to the glutathione conjugate by glutathione S-transferases (GSTs). It was accumulated in mammalian cells by up to several hundred-fold over the extracellular concentration, by conjugation with intracellular GSH. The induction of ARE by SFN was 8.6-fold higher than by SFN-NAC. The decrease in ARE expression at higher concentrations of SFN and SFN-NAC was correlated with the accelerated apoptotic cell death, with a dosedependent activation of caspase 3 activity by SFN. Upon addition of extracellular GSH within 6 hr of treatment with SFN, the effect on ARE expression was blocked almost completely.
목차
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS AND DISCUSSION
ACKNOWLEDGEMENTS
REFERENCES
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UCI(KEPA) : I410-ECN-0101-2009-511-018071595