RT Journal Article
SR Electronic
T1 Diallyl Disulfide (DADS) Induces Apoptosis in Human Cervical Cancer Ca Ski Cells <em>via</em> Reactive Oxygen Species and Ca<sup>2+</sup>-dependent Mitochondria-dependent Pathway
JF Anticancer Research
JO Anticancer Res
FD International Institute of Anticancer Research
SP 2791
OP 2799
VO 28
IS 5A
A1 LIN, YUH-TZY
A1 YANG, JAI-SING
A1 LIN, SHUW-YUAN
A1 TAN, TZU-WEI
A1 HO, CHIN-CHIN
A1 HSIA, TE-CHUN
A1 CHIU, TSAN-HUNG
A1 YU, CHUN-SHU
A1 LU, HSU-FENG
A1 WENG, YUEH-SHAN
A1 CHUNG, JING-GUNG
YR 2008
UL http://ar.iiarjournals.org/content/28/5A/2791.abstract
AB The mechanisms of apoptosis induced by diallyl disulfide (DADS) were explored in human cervical cancer Ca Ski cells. Flow cytometric analysis, DNA gel electrophoresis and DAPI staining demonstrated that DADS induced apoptosis in Ca Ski cells. DADS induced apoptosis through the production of reactive oxygen species and Ca2+, and induced abrogation of mitochondrial membrane potential (Δψm) and cleavage of Bid protein (t-Bid). DADS increased the levels of p53, p21 and Bax, but caused a decrease in the level of Bcl-2. DADS also promoted the activities of caspase-3 leading to DNA fragmentation, thus indicating that DADS-induced apoptosis is caspase-3 dependent. In addition, DADS induced an increase in the level of cytochrome c in the cytoplasm, which was released from mitochondria. BAPTA attenuated the Δψm abrogation and significantly diminished the occurrence of DADS-induced apoptosis in Ca Ski cells. In conclusion, DADS-induced apoptosis occurs via production of ROS and caspase-3 and a mitochondria-dependent pathway in Ca Ski cells.