Manganese superoxide dismutase (MnSOD) catalyzes NO-dependent tyrosine residue nitration
| Autor: | Vesna Niketić, B Mihajlo Spasic, Srdjan Stojanović, Milan Nikolić, Dragana Stanic, Smiljana Raicevic |
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| Rok vydání: | 2005 |
| Předmět: |
animal diseases
010402 general chemistry medicine.disease_cause 01 natural sciences peroxynitrite Nitric oxide lcsh:Chemistry 03 medical and health sciences chemistry.chemical_compound nitric oxide In vivo Nitration medicine Tyrosine 030304 developmental biology 3-nitrotyrosine chemistry.chemical_classification 0303 health sciences Superoxide fungi General Chemistry 0104 chemical sciences enzymes and coenzymes (carbohydrates) Enzyme lcsh:QD1-999 chemistry Biochemistry Peroxynitrite Oxidative stress mnsod |
| Zdroj: | Journal of the Serbian Chemical Society, Vol 70, Iss 4, Pp 601-608 (2005) |
| ISSN: | 1820-7421 0352-5139 |
| DOI: | 10.2298/jsc0504601s |
| Popis: | The peroxynitrite-induced nitration of manganese superoxide dismutase (MnSOD) tyrosine residue, which causes enzyme inactivation, is well established. This led to suggestions that MnSOD nitration and inactivation in vivo, detected in various diseases associated with oxidative stress and overproduction of nitric monoxide (NO), conditions which favor peroxynitrite formation, is also caused by peroxynitrite. However, our previous in vitro study demonstrated that exposure of MnSOD to NO led to NO conversion into nitrosonium (NO+) and nitroxyl (NO?) species, which caused enzyme modifications and inactivation. Here it is reported that MnSOD is tyrosine nitrated upon exposure to NO, as well as that MnSOD nitration contributes to inactivation of the enzyme. Collectively, these observations provide a compelling argument supporting the generation of nitrating species in MnSOD exposed to NO and shed a new light on MnSOD tyrosine nitration and inactivation in vivo. This may represent a novel mechanism by which MnSOD protects cell from deleterious effects associated with overproduction of NO. However, extensive MnSOD modification and inactivation associated with prolonged exposure to NO will amplify the toxic effects caused by increased cell superoxide and NO levels. |
| Databáze: | OpenAIRE |
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