Abstrakt: |
We estimated the cerebral oxidative stress during ischemia-reperfusion of the brain in conditions of modulated L-arginine-NO system in rats. In 128 rats, the changes in lipid peroxidation products (conjugated dienes, malondialdehyde, Schiff bases) and antioxidant defense factors (retinal, a-tocopherol, SH-groups) were studied. Analysis of the inhibitor (administration of NO synthase substrate L-arginine, non-selective inhibitor Nw-nitro-L-arginine methyl ester, selective inhibitor of neuronal NO synthase 7-nitroindasole, or selective inhibitor of inducible NO synthase S-methyl-isothiourea) showed the NO-dependent nature of oxidative stress in rats with brain ischemia-reperfusion. NO generated by different NO synthase isoenzymes played different roles: hyperactivation of the neuronal NO synthase was associated with oxidative stress during both brain ischemia-reperfusion periods, and the higher inducible NO synthase activity had such association only during the later period. |