Antioxidant Role of Sodium Selenite on Ammonium Sulphate Induced Oxidative Stress in Rats

Ammonia is an important source of nitrogen metabolism and it is necessary for synthesis of protein and amino acids. An excessive level of ammonia leads to disturbance in the physiological functions of the body. High concentrations of ammonia enter into the body, because of environmental pollution, urea cycle disorders, liver failure and ingestion of ammonium salts cause physiological disturbance and damage of organs. The present study is to investigate the possibilities of the protective role of Selenium in Ammonium Sulphate (AS)-induced stress in the rat brain and liver. Rats were divided into four groups (six animals in each group). Group I (GI) is served as control, Group II (AS) rats received 18.3 mg/kg b.w of ammonium sulphate via intraperitonially (i.p) injection, Group III (Ss) rats administered with Sodium selenite (0.3 mg/kg b.wi.p) and Group IV (AS + Ss) treated with both of AS (18.3 mg/kg bwi.p) plus Ss (0.3 mg/kg b.wi.p). Acute intoxication of AS treated rats has shown that significantly decreased levels of antioxidant enzymes; namely Superoxide dismutase (SOD), Catalase (CAT), Glutathione peroxidase (GPx), and increased levels of Xanthine oxidase (XOD) levels in brain and liver tissues. Treatments with Ss reversed the ASinduced alteration of antioxidant defence enzyme levels.Selenium administration might be scavenging the excess of ammonium ions and significantly prevent the oxidative stress in liver and brain.