Modulatory role of N-acetyl-cysteine on gastric mucosal lesions and some biochemical changes in Wistar rats subjected to cold restraint stress

Background: Gastric ulcer affects many people worldwide and it is caused by many factors such as stress, medications, particularly non- steroidal anti-inflammatory drugs, infections caused by Helicobacter pylori and Cytomegalovirus. Exposure to Cold restraint stress (CRS)  has been established to cause oxidative stress leading to cellular death. Nacetyl-cysteine (NAC) is an antioxidant that protects the lipid  bio-membrane against oxidative stress. This study investigated the effect NAC on gastric mucosal lesion and some biochemical changes  in Wistar rats subjected to CRS. Methodology: Sixteen (16) adult male rats were divided into four (4) groups; Group I (Control): Distilled  water/Kg Group II: Distilled water + CRS 3½ hrs (Ulcer group), Group III: NAC 500 mg/kg orally + CRS 3½ hrs Group IV: Ranitidine 50 mg/ kg + CRS 3½ hrs. All treatment lasted for 7 days while exposure to CRS was for 3½ hours on 7th day. Three hours after exposure of rats to  CRS, rats of all groups were euthanized under diazepam and ketamine anesthesia. The stomach and blood samples were collected for  physical and biochemical analysis. Data were analysed using ANOVA and p < 0.05 was considered significant. Results: The P index of NAC  in CRS induced ulcer was found to be 66.7 %. A significant increase (P = 0.001) in body weight was observed in CRS + Ranitidine group,  when compared to the control. A significant (P = 0.001) increase was observed in the INOS concentration in NAC + CRS, Ranitidine + CRS,  when compared to the control. Conclusion: We surmise that acute administration of NAC significantly increased body weight of rats  subjected to CRS. The high preventive index of N-acetyl cysteine on CRS induced ulcer was as the result of the antioxidant properties of  NAC which might have contributed to its’ gastro protection against gastric mucosal lesions.