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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
- 학술저널
- 저자정보
- 발행연도
- 2002.1
- 수록면
- 10 - 257 (248page)
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Diallyl disulfide (DADS) induced apoptosis throughthe caspase-3 dependent pathway in leukemia cellswas earlier reported from this laboratory. In thisstudy, we investigated the involvement of Ca2+ inDADS-induced apoptotic cell death of HCT-15,human colon cancer cell line. DADS induced the ele-vation of cytosolic Ca2+ by biphasic patern; rapidCa2+ peak at 3 min and following slow and sustainedelevation till 3 h after the addition of DADS. Produc-tion of H2O2 was also observed with its peak value at4 h. Apoptotic pathways including the sequence ofcaspase-3 activation, poly(ADP-ribose) polymerasecleavage, and DNA fragmentation by DADS werecompletely blocked by various inhibitors such asspecific caspase-3 inhibitor, free radical scavenger,and intracellular Ca2+ chelator. N-acetylcystein andcatalase treatment prevented the accumulation ofH2O2 and later caspase-3 dependent apoptotic path-way. However, these radical scavengers did notblock the elevation of intracellular Ca2+. Treatment of cells with 1,2-bis(2-aminophenoxy-ethane)-N,N,N-tetraacetic acid tetrakis -acetoxymethylester (BAPTA-AM), cellular Ca2+ chelator, resulted in acomplete blockage of the caspase-3 dependent apop-totic pathway of HCT-15 cells. It abolished the elevationof intracellular Ca2+, and furthermore, completely inhib-ited the production of H 2O2. These results indicate thatcytosolic Ca2+ elevation is an earlier signaling event inapoptosis of HCT-15 cells. Collectively, our data dem-onstrate that DADS can induce apoptosis in HCT-15cells through the sequential mechanism of Ca2+homeostasis disruption, accumulation of H 2O2, andresulting caspase-3 activation.
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