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      저자 : Eun-ChungJhee (검색결과 1 건)
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        Role of Ca2+ in diallyl disulfide-induced apoptotic cell death of HCT-15 cells

        Eun-KyungPark,권강범,Kie-InPark,Byung-HyunPark,Eun-ChungJhee 생화학분자생물학회 2002 Experimental and molecular medicine Vol.34 No.3

        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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