期刊
LEUKEMIA RESEARCH
卷 33, 期 1, 页码 151-158出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.leukres.2008.07.009
关键词
Oxidative stress; Apoptosis; c-Jun N-terminal kinase; Chemotherapy; Mitochondria; Calcium
资金
- National Institute of Biomedical Innovation (NIBIO)
Leukemic cell apoptosis may be enhanced by appropriate oxidative stress. We report here the mechanism of Jurkat cell apoptosis by monochloramine (NH2Cl), a neutrophil-derived oxidant. NH2Cl induced caspase-dependent apoptosis, which was preceded by cytochrome c and Smac/Diablo release from mitochondfia. Within 10 min of NH2Cl treatment, c-Jun N-terminal kinase (JNK) activation and elevation of cytosolic Ca2+ were observed. JNK inhibitors (SP600125 or JNK inhibitor VIII) significantly suppressed the apoptosis as well as caspase cleavage and cytochrome c release. In contrast, Ca2+ chelation by EGTA + acetoxymethyl-EGTA had no effects on apoptosis. Our results indicated that JNK activation contributed most importantly to the NH2Cl-induced apoptosis. (C) 2008 Elsevier Ltd. All fights reserved.
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