title: Regulation of apoptosis by nitrosative stress.
abstract: Nitrosative stress can prevent or induce apoptosis. It occurs via S-nitrosylation by the interaction of nitric oxide (NO) with the biological thiols of proteins. Cellular redox potential and non-heme iron content determine S-nitrosylation. Apoptotic cell death is inhibited by S-nitrosylation of the redox-sensitive thiol in the catalytic site of caspase family proteases, which play an essential role in the apoptotic signal cascade. Nitrosative stress can also promote apoptosis by the activation of mitochondrial apoptotic pathways, such as the release of cytochrome c, an apoptosis-inducing factor, and endonuclease G from mitochondria, as well as the suppression of NF-kB activity. In this article we reviewed the mechanisms whereby S-nitrosylation and nitrosative stress regulate the apoptotic signal cascade.
authors.affiliation: Vascular System Research Center, Kangwon National University, Chunchon, Kangwon-do, Korea.
authors.forename: Ki-Mo
authors.initials: KM
authors.lastname: Kim
authors.forename: Peter K M
authors.initials: PK
authors.lastname: Kim
authors.forename: Young-Guen
authors.initials: YG
authors.lastname: Kwon
authors.forename: Se-Kyung
authors.initials: SK
authors.lastname: Bai
authors.forename: Woo-Dong
authors.initials: WD
authors.lastname: Nam
authors.forename: Young-Myeong
authors.initials: YM
authors.lastname: Kim
mesh_terms: D000818:Animals; D017209:Apoptosis; D061945:Caspase Inhibitors; D016923:Cell Death; D006418:Heme / Q000737:chemistry; D006801:Humans; D007501:Iron / Q000378:metabolism; D008928:Mitochondria / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism*; D009584:Nitrogen / Q000378:metabolism*; D010084:Oxidation-Reduction; D015398:Signal Transduction; D013438:Sulfhydryl Compounds / Q000737:chemistry
chemical_list: D061945:Caspase Inhibitors; D013438:Sulfhydryl Compounds; D009569:Nitric Oxide; D006418:Heme; D007501:Iron; D009584:Nitrogen