Effect of Ammonium Stress on Carbohydrate Metabolism in the Brain and Liver of Rat: Mitigation Role of Selenium

Abstract

All living organisms produce ammonia as a byproduct of cellular metabolism. However, at higher concentration it is toxic and leads to deleterious effects on cellular metabolic functions. But ammonia is essential for synthesis of many compounds in the body like amino acids, purines, pyrimidines, amino sugars, asparagine etc when it is at optimum levels. Excess ammonia is excreted mainly as urea, which is synthesized in the liver through urea cycle. Ammonia is a normal constituent of all body fluids, but can become a toxicant under ammonia stress, which leads to ammonia toxicity or Hyperammonemia. In this condition, metabolic mechanisms are disturbed. 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 a 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.w;i.p) and Group IV (As + Ss) treated with both of As (18.3 mg/kg b.w;i.p) plus Ss (0.3 mg/kg b.w;i.p). Acute intoxication of As treated rats have shown that significantly increased levels of carbohydrates; namely Glucose, Lactate and decreased levels of Glycogen and Pyruvate levels in brain and liver tissues. Treatments with Ss reversed the As induced alteration of carbohydrates levels.