Abstract

Background: Ammonia is an important source of nitrogen metabolism and it is necessary for the synthesis of protein and amino acids. An excessive level of ammonia leads to disturbing the physiological functions of the body, causes to increase the free radical levels in tissues and body fluids, its reveal that damage of tissue by reactive oxygen species (ROS) changes of acid-base lances in the body fluid’s causes’ physiological disturbance and damage of organs. Aims and Objectives: The present study was conducted to assess the mitigating role of zinc on ammonium sulfate (AS)-induced biochemical alterations (lipid peroxidation [LPO] and antioxidants) in rat liver and muscle.
Materials and Methods: Rats were divided into four groups (six animals in each group). Group I (GI) served as control and rats provided with normal diet and water, Group II (AS) rats treated intraperitoneal (i.p) with 18.3 mg/kg b.w of AS, Group III (zinc chloride [Zc]) rats administered with Zc (4 mg/kg b.w i.p), and Group IV (AS + Zc) treated with both of AS (18.3 mg/kg bwi.p) plus Zc (4 mg/kg b.w i.p) Zc given after 1 h dosage of AS.
Results: In the present investigation, AS-treated animals showed a significant increase in the levels of LPO and declined levels of selected antioxidants such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione reductase (GR) levels in the liver and muscle of rats. On the other hand, only zinc-treated rats (Zc) showed no significant variations in LPO and antioxidants in the liver and muscle. However, in AS + Zc treated animals, elevated levels of LPO and decreased SOD, CAT, GPx, and GR antioxidant levels were reversed to normal when compared with AS-treated rats. Conclusion: Accordingly, these findings suggest that zinc supplementation significantly inhibits the oxidative stress in hepatic cells and muscle cells in AS toxicity