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To examine the protective effect of melatonin, cytotoxicity assay, DNA fragmentation analysis, caspase\u20103 activity assay, and Western blotting for caspase\u20103 and poly(ADP\u2010ribose) polymerase (PARP) were performed. Treatment of cells with <jats:italic>S<\/jats:italic>\u2010nitroso\u2010<jats:italic>N<\/jats:italic>\u2010acetylpenicillamine (SNAP), an NO donor, was shown to induce apoptotic cell death in a dose\u2010dependent manner, and pretreatment with melatonin (0.1\u2003m<jats:sc>m<\/jats:sc>) attenuated the occurrence of NO\u2010induced apoptotic cell death. DNA fragmentation in response to NO was also arrested by melatonin. Caspase\u20103 activity induced by NO was decreased with melatonin treatment. Furthermore, the active fragments of caspase\u20103 and PARP were almost completely absent following exposure to melatonin. To elucidate the protective mechanisms of action of melatonin, Western blot analyses for Bcl\u20102 expression and cytochrome c release were carried out. Pretreatment with melatonin (0.1\u2003m<jats:sc>m<\/jats:sc>) induced the expression of Bcl\u20102 and suppressed the release of cytochrome c into the cytosol, thereby arresting NO\u2010induced apoptotic cell death. These results suggest that the antiapoptotic effect of melatonin is associated with induction of Bcl\u20102 expression in PGT\u2010\u03b2 cells, which in turn blocks caspase\u20103 activation and inhibits cytochrome c release into the cytosol.<\/jats:p>","DOI":"10.1034\/j.1600-079x.2002.02899.x","type":"journal-article","created":{"date-parts":[[2003,3,12]],"date-time":"2003-03-12T08:32:40Z","timestamp":1047457960000},"page":"146-150","source":"Crossref","is-referenced-by-count":57,"title":["Melatonin suppresses NO\u2010induced apoptosis via induction of Bcl\u20102 expression in PGT\u2010\u03b2 immortalized pineal 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