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J Biol Chem, Vol. 273, Issue 51, 34272-34277, December 18, 1998
,§,,,,
From the Nitric oxide (NO) is implicated in apoptosis and
has both cytotoxic and cytoprotective effects. Exogenous NO induced the
death of PC12 and HeLa cells via a process showing features of both apoptosis and necrosis, with chromatin condensation, nuclear
compaction, and mitochondrial swelling. Activation of caspases was not
observed during NO-induced cell death. In addition, cell death was not inhibited by peptide caspase inhibitors or by expression of
p35, a baculovirus-encoded caspase inhibitor, indicating
that NO-induced cell death was independent of caspases. NO-induced cell
death was enhanced by Bax expression in a caspase-independent manner and prevented by the anti-cell death protein Bcl-2. Although Bcl-2 has
previously been shown to prevent cell death by inhibiting caspase
activation, these results indicate that it can also prevent cell death
via a caspase-independent mechanism.
The First Department of Surgery,
§ Department of Medical Genetics, Biomedical Research
Center, Osaka University Medical School, 2-2 Yamadaoka, Suita, Osaka
565-0871 Japan
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