ABSTRACT
Chronic ethanol and paracetamol consumption, both individually and in combination, caused hepatic changes in rats. Treatment of testosterone (2.5 mg/kg body wt.) to the alcoholic and paracetamol administered rats showed decreased activities of serum transaminases, serum acid and alkaline phosphatases, and decreased levels of hepatic triglycerides, cholesterol and free fatty acids. Concentration of the lipid peroxidation product-malondialdehyde was significantly decreased in the liver after testosterone treatment in alcohol and paracetamol administered groups. Histopathological observations further confirm that testosterone could offer protection against alcohol and paracetamol induced damage to liver in animals.
Subject(s)
Acetaminophen/antagonists & inhibitors , Animals , Body Weight , Eating , Ethanol/antagonists & inhibitors , Lipid Metabolism , Liver/drug effects , Male , Rats , Rats, Sprague-Dawley , Testosterone/pharmacologyABSTRACT
Ethanol administration to rats for 30 days and 90 days followed by paracetamol administration resulted in liver injury indicated by the significant increase in the serum GOT and GPT levels. The ethanol treatment to rats and the administration of paracetamol to the normal and alcoholic rats also caused a significant increase in the activity of serum acid and alkaline phosphatase. The hepatotoxicity of ethanol and paracetamol were indicated by the histological alterations in this study. The content of lipid peroxidation products-malondialdehyde, hydroperoxides and conjugated dienes were increased in the liver, heart, kidney and brain of the acute and chronic ethanol treated and paracetamol treated rats. The activities of the antiperoxidative enzymes-SOD and catalase decreased in the ethanol and paracetamol treated rats. The changes in the activities of the antiperoxidative enzymes in alcoholism and drug toxicity suggests increased peroxidation, increased synthesis of ecosonoids and increased damage to the tissues. The glutathione levels were decreased in the rats administered ethanol for 30 days, while the glutathione levels increased in the 90 days ethanol treated rats. The paracetamol treatment caused a decrease in the glutathione levels in the normals and the ethanol treated rats.