PROTECTIVE EFFECT OF DEFEROXAMINE ON SODIUM NITROPRUSSIDE-INDUCED APOPTOSIS IN PC12 CELLS

Reportedly, the generation of nitric oxide (NO) may lead to iron mobil ization from ferritin disrupting intracellular iron homeostasis and in creasing levels of reactive oxygen species. In the present study, we e valuated the role of endogenous iron in NO-induced apoptosis in PC12 c ells. Apoptosis was tested by flow cytometry, fluorescence microscopy and terminal deoxynucleotidyl transferase-mediated 2'-deoxy-uridine 5' -triphosphate nick end labeling (TUNEL) technique. Cell viability was determined by (4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromi de (MTT) assay. When incubated with 0.5-0.75 mM sodium nitroprusside ( SNP, a chemical NO donor), PC12 cells were shown to undergo apoptosis. In addition, SNP induced a time-dependent decrease in cell viability. Since deferoxamine (0.05-0.1 mM), a powerful iron chelator, inhibited both SNP-induced apoptosis and the decrease in cell viability, we sug gest that these NO effects may be dependent upon iron mobilization wit hin the cell. (C) 1998 Elsevier Science Ireland Ltd.