The degree of oxidative stress in the rat brain during ischemia and reperfusion in conditions of correction of the L-arginine-NO system.
The aim of the present work was to evaluate oxidative stress in the brains of rats during ischemia/reperfusion in conditions of correction of the L-arginine-NO system. Experiments on 128 rats with brain ischemia/perfusion in conditions of modulation of the L-arginine-NO system were used to study changes in the concentrations of (a) lipid peroxidation products, i.e., diene conjugates, malonic dialdehyde, and Schiff bases, and (b) antioxidant protection factors, i.e., retinol, alpha-tocopherol, and SH-groups. Administration of L-arginine and NO synthase inhibitors, i.e., the non-selective inhibitor N(omega)-nitro-L-arginine methyl ester, the selective neuronal NO synthase inhibitor 7-nitroindasole, and the selective inhibitor of inducible NO synthase S-methylisothiourea, established that oxidative stress in rats with brain ischemia/perfusion is NO-dependent. NO formed by the various isoforms of NO synthase had different roles: hyperactivation of neuronal NO synthase was responsible for oxidative stress in both periods of brain ischemia/reperfusion, while increased inducible NO synthase activity was responsible in the late period.
Maksimovich
N E
NE
Department of Pathophysiology, Grodno State Medical University, Belarus.
Zinchuk
V V
VV
Maslakov
D A
DA
D000818:Animals; D001120:Arginine / Q000378:metabolism*; D001921:Brain / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D004195:Disease Models, Animal; D004791:Enzyme Inhibitors / Q000494:pharmacology; D015227:Lipid Peroxidation / Q000187:drug effects / Q000502:physiology; D008297:Male; D009569:Nitric Oxide / Q000378:metabolism*; D018384:Oxidative Stress / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D015427:Reperfusion Injury / Q000188:drug therapy / Q000503:physiopathology*; D014815:Vitamins / Q000494:pharmacology
D004791:Enzyme Inhibitors; D014815:Vitamins; D009569:Nitric Oxide; D001120:Arginine