Asunto(s)
Humanos , Anestésicos por Inhalación/efectos adversos , Metilenotetrahidrofolato Reductasa (NADPH2)/deficiencia , Homocistinuria/diagnóstico , Anestesia , Espasticidad Muscular/diagnóstico , Óxido Nitroso/efectos adversos , Trastornos Psicóticos/diagnóstico , Trastornos Psicóticos/genética , 5-Metiltetrahidrofolato-Homocisteína S-Metiltransferasa/antagonistas & inhibidores , Cuidados Preoperatorios , Hiperhomocisteinemia/complicaciones , Metilenotetrahidrofolato Reductasa (NADPH2)/genética , Homocisteína S-Metiltransferasa/metabolismo , Homocistinuria/genética , Espasticidad Muscular/genética , MutaciónRESUMEN
Inactivation of methionine synthase (MS) by nitrous oxide (N2O) administration to animals and man has been postulated to be mediated by hydroxyl radical (OH). An alternate mechanism has been proposed which involves superoxide radical (O2.-) originating from N2O in the inactivation of MS by OH that may arise from O2.- through Fenton/Haber-Weiss reaction. Rats inhaling a mixture of N2O:O2 (1:1) for 5 hr showed inactivation of MS in liver to nearly 90% which could not be reversed by prior administration of either dimethyl sulfoxide (DMSO) or sodium benzoate. Pretreatment of rats with superoxide dismutase (SOD) at two doses, 0.1 mg and 3.5 mg/100 g body weight, retarded the in vivo inactivation of MS by N2O, to 76% and 47% respectively. In vitro inactivation of MS with N2O could not be retarded by DMSO or Na-benzoate, or either exogenous SOD or catalase.