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Objective: To investigate the possible mechanisms of splenozide influence on oxidative stress and metabolic disorders in tissues caused by acute nitrite intoxication in rats. Materials and Methods : Nitrite poisoning (NaNO2, 60 mg/kg, s.c.) was induced in rats pretreated with splenozide (natural metabolite, nucleoside complex; 3 mg/kg, i.p.). The parameters of lipid peroxidation (LPO), antioxidant defense system (superoxide dismutase [SOD], catalase [CAT], glutathione content [GSH], glutathione reductase [GR], glutathione peroxidase [GPx], glucose-6-phosphate dehydrogenase [G6PDH]), lactate and pyruvate concentrations, NAD+/NADH ratio in cytosol and mitochondrial succinate dehydrogenase (SDH) activity were evaluated in the liver, myocardium and brain. Results: Splenozide pretreatment decreased LPO, stimulated the G6PDH, GR and GPx activity, and increased the intracellular glutathione level in all studied tissues. Its effect on SOD, CAT and SDH activity depended on the type of tissue studied. Splenozide caused a reduction of lactate concentration and accumulation of oxidized NAD in cytosol. Conclusion: Splenozide demonstrated a weak scavenging activity against 1,1-diphenyl-2-picrylhydrazyl (DPPH) free radicals in vitro . Its antioxidant effect during nitrite intoxication may be due to the maintenance of glutathione recycling activity through the activation of NADPH-dependent reactions, redox state restoration and antiacidotic effect.

Role of complex nucleosides in the reversal of oxidative stress and metabolic disorders induced by acute nitrite poisoning