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In addition, t\u2010BOOH exposure induced activation of CPP32, as demonstrated by poly\u2010(ADP\u2010ribose) polymerase (PARP) cleavage, and of ICH\u20101L caspases. Exposure to t\u2010BOOH also induced a time\u2010dependent release of cytochrome c. Interestingly, in the presence of BAPTA, CPP32 activation still occurred, whereas ICH\u20101L activation was blocked. Ac\u2010DEVD\u2010CHO, an inhibitor of CPP32 activity, prevented the appearance of apoptotic cells, whereas the inhibitor of ICH\u20101L activity Z\u2010VDVAD\u2010FMK did not. Collectively, these findings demonstrate that in SH\u2010SY5Y neuroblastoma cells exposure to continuous and long\u2010lasting oxidative stress induced activation of caspase\u20103 that was independent of intracellular Ca<jats:sup>2+<\/jats:sup> ion concentration ([Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>) elevation but led to cell apoptosis. In contrast, caspase\u20102 activation was dependent on [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub> increase but did not result in apoptosis. \u00a9 2002 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jnr.10199","type":"journal-article","created":{"date-parts":[[2002,8,25]],"date-time":"2002-08-25T23:24:15Z","timestamp":1030317855000},"page":"454-462","source":"Crossref","is-referenced-by-count":26,"title":["Ca<sup>2+<\/sup>\u2010independent caspase\u20103 but not Ca<sup>2+<\/sup>\u2010dependent caspase\u20102 activation induced by oxidative stress leads to SH\u2010SY5Y human neuroblastoma cell 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