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Arginine, preadministered intraperitoneally at a dose of 120 mg per 100 g of body mass before hypoxia, decreased content of diene conjugates by 42-64% and Schiff bases by 7-15% in rat liver and testicular microsomal membranes as compared with control rats nontreated with arginine. Under these conditions cytochrome P-450 catalytic activity with aniline as a substrate was increased by 65-152% and with amidopyrine as a substrate--by 72-148%, respectively. Exogenous arginine inhibited an increase in membranes microviscosity, specific for hypoxic state; relative microviscosity of lipid bilayer was decreased by 36% and of the protein-lipid contact zones--by 84% as compared with control hypoxic animals.

A single intraperitoneal arginine injection increases the amidopyrin demethylation on 230% and aniline hydroxylation on 74% in rat liver microsomes. For all this the rate of lipid peroxidation estimated by the number of dienic conjugates and Schiff bases does not change. At the same time the exogenous arginine decreases the lipid bilayer microviscosity on 35% and increases the degree of protein submersion into lipid matrix on 54%. The experiments in vitro confirm the fact of activation in cytochrome P-450 isoform by arginine. A possible arginine effect on microsome membrane is under discussion.

Arginine (0.5 and 1 mu mol) decreased by 14-17% rates of superoxide anion formation in two systems: HADH-phenazine methosulfate and hydroxylamine autooxidation with nitrotetrazolium blue. These concentrations of arginine decreased by 40-50% formation of diene conjugates and Schiff bases in plasma when lipid peroxidation initiated by iron -ascorbate. Arginine administration before hypoxia decreased lipid peroxidation rate in plasma and liver microsomal membranes of rats.

Cold exposition within 3 days at 2-4 degrees caused destabilization of rat erythrocyte membranes. Content of blood serum hemoglobin, total peroxidase activity and the glucose-6-phosphate dehydrogenase activity were increased. Resistance of the animals against high oxygen pressure was reduced. Administration of arginine within 3 days into the animals led to stabilization of membranes and to elevation of rat resistance towards high oxygen pressure.

Activity of glutaminase (both phosphate-dependent and phosphate-independent forms of the enzyme) as well as glutamate decarboxylase activity were studied in hyperoxia (6 ati) and under conditions of protection by means of arginine from the effect of hyperoxia. In hyperoxia activity of phosphate-dependent and phosphate-independent forms of glutaminase was decreased by 45% and 51%, respectively. At the same time, glutamate decarboxylase activity was decreased by 32%. Arginine showed a protective effect, delaying the time of oxygen convulsions onset by 2.5-fold. The low activities of glutaminases were maintained but the glutamate decarboxylase activity was increased and even exceeded the control level by 29%. A mechanism of the protective effect of arginine is discussed.