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

Abstract

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 (NaNO 2 , 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 Department of Hypoxic States, 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.

The protective potential of Yucca schidigera (Sarsaponin 30®) against nitrite-induced oxidative stress in rats

“…The control group was given only 0.9% saline at the same volume. The rats were anesthetized and killed by cervical dislocation 50 min after the injection, when methemoglobin formation was at its peak [4]. Blood samples and organs including lung, liver, and kidney were collected for examination of clinical biochemistry.…”

“…Despite these beneficial effects, supernormal concentrations of nitrites in living organisms cause life-threatening states [4]. Acute nitrite intoxication is manifested primarily by methemoglobin (MetHb) formation (nitrite ion in contact with RBC (red blood cells) oxidizes ferrous iron in hemoglobin to the ferric state, forming stable MetHb which is incapable of oxygen transport) and resultant hypoxia [5], and mice [6] and rats [7,8] exposed to sodium nitrite were shown to achieve elevated concentrations of MetHb in their blood.…”

“…Nitrite methemoglobinemia is a potent process involving free radical generation [4]. Normal cellular function depends on a balance between reactive oxygen species (ROS) produced and antioxidant defense mechanisms available to the cell.…”

Comparative Studies on Turmeric and Vitamin C on Sodium Nitrite treated Rats

“…On other hand, there were significant decrease (p ≤ 0.05), in glutathione reductase , these findings are consistent with (Krishnamoorthy and Sangeetha, 2008) found that LPO level increased due to sodium nitrite administration but vitamin C treatment significantly reduced the lipid peroxidation level and nitrite content (Santos et al, 2009) . Gonchar et al (2006) said that over dose of nitrite caused decrease in glutathione reductase (GR). Vitamin C treated rats showed significant decrease in LPO as compared to sodium nitrite treated group.…”

Role of Natural Antioxidants in the Modulation of Plasma Amino Acid Pattern in Rats Exposed to Hemic Hypoxia

“…The branched chain amino acids (BCAAs), which include leucine, isoleucine, and valine, are readily metabolized in the muscle (Elwyn 1970), while aromatic amino acids (AAAs), which include phenylalanine and tyrosine are degraded in the liver. The plasma level of this latter group can be an indicator of tissue damage (Gonchar et al 2006). …”