期刊
FREE RADICAL BIOLOGY AND MEDICINE
卷 30, 期 9, 页码 1008-1018出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/S0891-5849(01)00493-2
关键词
hydrogen peroxide; glutathione; necrosis; homeostasis; desferrioxamine; dipyridyl; free radicals
资金
- NIA NIH HHS [1RO1-AG16718] Funding Source: Medline
Apoptosis was studied under conditions that mimic the steady state of H2O2 in vivo. This is at variance with previous studies involving a bolus addition of H2O2, a procedure that disrupts the cellular homeostasis. The results allowed us to define three phases for H2O2-induced apoptosis in Jurkat T-cells with reference to cytosolic steady state concentrations of H2O2 [(H2O2)(ss)] (H2O2)(ss) values below 0.7 muM elicited no effects: (H2O2)(ss) approximate to 0.7-3 muM induced apoptosis; and (H2O2)(ss) > 3 muM yielded no additional apoptosis and a gradual shift towards necrosis as the mode of cell death were observed. H2O2-induced apoptosis was not affected by either BCNU, an inhibitor of glutathione reductase, or diamide, a compound that reacts both with low-molecular weight and protein thiols, or selenols. Glutathione depletion, accomplished by incubating cells either with buthionine sulfoximine or in cystine-free medium, rendered cells more sensitive to H2O2-induced apoptosis, but did not change the threshold and saturating concentrations of H2O2 that induced apoptosis. Two unrelated metal chelators, desferrioxamine and dipyridyl, strongly protected against H2O2-induced apoptosis. It may be concluded that, under conditions of H2O2 delivery that mimic in vivo situations, the oxidative event that triggers the induction of apoptosis by H2O2 is a Fenton-type reaction and is independent of the thiol or selenium states of the cell. (C) 2001 Elsevier Science Inc.
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