title: Partial Protection of PC12 Cells from Cellular Stress by Low-Dose Sodium Nitroprusside Pre-treatment.
abstract: The PC12 rat pheochromocytoma cell line is an in vitro model system widely used for the investigation of intracellular signaling events contributing to neuronal differentiation and cell death. We found earlier that the nitric oxide donor compound sodium nitroprusside (SNP) induced apoptosis of PC12 cells if it was applied in high concentration (400 µM). Yoshioka et al. (J Pharmacol Sci 101:126-134, 2006) reported that cell death evoked by cytotoxic concentrations of SNP could be prevented by a 100 µM SNP pre-treatment in a murine macrophage cell line. The apoptosis caused by toxic-dose SNP treatment (400 µM) could be partially overcome in PC12 cells as well by the low-dose SNP pre-treatment. The partial inhibition of apoptosis was accompanied by reduced phosphorylation of certain proteins (such as stress-activated protein kinases, the p53, and the eIF2α proteins), decreased caspase activation, and less intense internucleosomal DNA fragmentation. The 100 µM SNP pre-treatment reduced the pro-apoptotic potential of certain other stress stimuli (serum withdrawal, cisplatin and tunicamycin treatments) as well, although the underlying biochemical changes were not entirely uniform. On the contrary, the 100 µM SNP pre-treatment was unable to prevent cell death caused by the protein synthesis inhibitor anisomycin. Further clarification of the above-mentioned processes may be important in understanding the mechanisms by which mild nitrosative stress protects cells against certain forms of cellular stress conditions.
authors.affiliation: Department of Medical Biology, Medical School, University of Pécs, Szigeti út 12., Pecs, 7624, Hungary.|Signal Transduction Research Group, Szentágothai Research Centre, Ifjúság útja 20., Pecs, 7624, Hungary.
authors.forename: Judit
authors.initials: J
authors.lastname: Varga
authors.affiliation: Department of Medical Biology, Medical School, University of Pécs, Szigeti út 12., Pecs, 7624, Hungary.|Signal Transduction Research Group, Szentágothai Research Centre, Ifjúság útja 20., Pecs, 7624, Hungary.
authors.forename: Judit
authors.initials: J
authors.lastname: Bátor
authors.affiliation: Department of Medical Biology, Medical School, University of Pécs, Szigeti út 12., Pecs, 7624, Hungary.
authors.forename: Gergő
authors.initials: G
authors.lastname: Nádasdi
authors.affiliation: Department of Medical Biology, Medical School, University of Pécs, Szigeti út 12., Pecs, 7624, Hungary.|Signal Transduction Research Group, Szentágothai Research Centre, Ifjúság útja 20., Pecs, 7624, Hungary.
authors.forename: Zita
authors.initials: Z
authors.lastname: Árvai
authors.affiliation: Department of Medical Biology, Medical School, University of Pécs, Szigeti út 12., Pecs, 7624, Hungary.|Signal Transduction Research Group, Szentágothai Research Centre, Ifjúság útja 20., Pecs, 7624, Hungary.
authors.forename: Renáta
authors.initials: R
authors.lastname: Schipp
authors.affiliation: Department of Medical Biology, Medical School, University of Pécs, Szigeti út 12., Pecs, 7624, Hungary. jozsef.szeberenyi@aok.pte.hu.|Signal Transduction Research Group, Szentágothai Research Centre, Ifjúság útja 20., Pecs, 7624, Hungary. jozsef.szeberenyi@aok.pte.hu.
authors.forename: József
authors.initials: J
authors.lastname: Szeberényi
mesh_terms: D000818:Animals; D053148:Caspase 3; D016923:Cell Death / Q000187:drug effects; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects; D045304:Cytochromes c / Q000378:metabolism; D053938:DNA Fragmentation / Q000187:drug effects; D020030:Nitric Oxide Donors / Q000494:pharmacology*; D009599:Nitroprusside / Q000494:pharmacology*; D016716:PC12 Cells; D051381:Rats; D015398:Signal Transduction / Q000187:drug effects*; D013312:Stress, Physiological
chemical_list: D020030:Nitric Oxide Donors; D009599:Nitroprusside; D045304:Cytochromes c; C505410:Casp3 protein, rat; D053148:Caspase 3
keywords: Apoptosis; Cellular stress; Nitric oxide; PC12 cells