RESUMO
This paper describes the O(2)-dependent control of the reactivity of nitrogen oxide species for the production of biologically important nitrated and nitrosated compounds. In this study, the effects of O(2) on the reactivity of NO, NO(2), and ONOO(-)/ONOOH for nitration of tyrosine (Tyr) and nitrosation of glutathione (GSH) and morpholine (MOR) were examined. NO produced S-nitrosoglutathione (GSNO) and N-nitrosomorpholine (NMOR) through the formation of N(2)O(3) under aerobic conditions, and NO(2) produced 3-nitrotyrosine (3-NO(2)Tyr), GSNO, and NMOR. Transnitrosation from GSNO to MOR was observed only in the presence of O(2). Although preformed ONOO(-)/ONOOH produced all the products under aerobic conditions, the formation of 3-NO(2)Tyr and GSNO was markedly reduced and the formation of NMOR was enhanced under anaerobic conditions. The reactivity of the CO(2) adduct of ONOO(-) was similarly dependent on O(2). 3-NO(2)Tyr was produced effectively by reaction with ONOO(-)/ONOOH at the O(2) concentration of 270 microM and by reaction with its CO(2) adduct at O(2) concentrations greater than 5 microM. Generation of.OH from ONOO(-)/ONOOH was suppressed under anaerobic conditions. The reactivity of ONOO(-)/ONOOH and.OH generation from ONOO(-) were reversibly controlled by the O(2) concentration.
Assuntos
Óxidos de Nitrogênio/química , Oxigênio/química , Ácido Peroxinitroso/química , Tirosina/análogos & derivados , Anaerobiose , Espectroscopia de Ressonância de Spin Eletrônica , Glutationa/química , Molsidomina/análogos & derivados , Molsidomina/química , Morfolinas/química , Óxido Nítrico/química , Nitrosaminas/química , Óxido Nitroso/química , S-Nitrosoglutationa/química , Soluções , Tirosina/químicaRESUMO
Antioxidant and prooxidant effects of nitric oxide (NO) on lipid peroxidation in aqueous and non-aqueous media were examined. In an aqueous solution, NO did not induce peroxidation of unoxidized methyl linoleate (ML) and suppressed the radical initiator-induced oxidation of ML. NO suppressed the Fe(II) ion-induced oxidation of mouse liver microsomes. NO reduced the O2 consumption during the radical initiator-induced oxidation of linoleic acid in an aqueous medium. NO conversion into NO2- in an aqueous medium was not affected by unoxidized ML and was slightly reduced by peroxidizing ML. On the other hand, as well as pure NO2, NO induced peroxidation of unoxidized ML in n-hexane in a dose-dependent fashion. NO did not suppress the radical initiator-induced oxidation of ML in n-hexane. Nitrogen oxide species (NO2 or N2O3) formed by autoxidation was dramatically lost in n-hexane in the presence of unoxidized ML. The results indicated that NO terminated lipid peroxidation in an aqueous medium, whereas NO induced lipid peroxidatiton in a non-aqueous medium. Hence, NO showed both antioxidant and prooxidant effects on lipid peroxidation depending on the solvents.
