Activation of c-Jun N-terminal kinase is essential for oxidative stress-induced Jurkat cell apoptosis by monochloramine.

Abstract:

:Leukemic cell apoptosis may be enhanced by appropriate oxidative stress. We report here the mechanism of Jurkat cell apoptosis by monochloramine (NH(2)Cl), a neutrophil-derived oxidant. NH(2)Cl induced caspase-dependent apoptosis, which was preceded by cytochrome c and Smac/Diablo release from mitochondria. Within 10min of NH(2)Cl treatment, c-Jun N-terminal kinase (JNK) activation and elevation of cytosolic Ca(2+) were observed. JNK inhibitors (SP600125 or JNK inhibitor VIII) significantly suppressed the apoptosis as well as caspase cleavage and cytochrome c release. In contrast, Ca(2+) chelation by EGTA+acetoxymethyl-EGTA had no effects on apoptosis. Our results indicated that JNK activation contributed most importantly to the NH(2)Cl-induced apoptosis.

journal_name

Leuk Res

journal_title

Leukemia research

authors

Ogino T,Ozaki M,Hosako M,Omori M,Okada S,Matsukawa A

doi

10.1016/j.leukres.2008.07.009

subject

Has Abstract

pub_date

2009-01-01 00:00:00

pages

151-8

issue

1

eissn

0145-2126

issn

1873-5835

pii

S0145-2126(08)00338-X

journal_volume

33

pub_type

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