Regulation of Trace Elements by Vitamin A in Paracetamol-induced Liver Toxicity in Rats

This study was aiming to determine the effect of the Vitamin A on paracetamol-induced hepatotoxicity. Fifteen rats were randomly divided into five groups; (three rats each) control group, paracetamol (1000 mg/kg body weight) was used to induce hepatotoxicity in albino rats. Vitamin A (Retinyl palmtate) administered at the dose levels of 100, 500 and1000 IU/kg body weights orally for 7 days prior to paracetamol dose. Hepatic toxicity was observed in paracetamol group; aspartate aminotransaminase (AST) level was high as compared with control group (p = 0.003). The significant hepatoprotective effect of Vitamin A was observed at doses 500 and 1000 IU/kg body weight, as there was significant reduction of serum AST when compared to paracetamol group (p = 0.01 and 0.003 respectivly), where 100 IU/Kg vitamin A not significantly decrease AST. Liver trace element determined by X-ray fluorescence (XRF) (K, Ca, Fe, Cu, Zn and Rb) in paracetamol-treated group were found to be higher than that of the control group, although the only significant increase was observed with Cu. Br shows slight decrease compared to the control group. There were no significant differences between Vitamin A groups (100 mg/kg 500mg/kg and 1000mg/kg) and PCM-treated group in the liver tissue content of Ca, K, Zn, Cu, Rb and Br where Fe concentrations were significantly decrease at doses 500 and 1000IU/l (P value 0.05 and 0.045 respectively). Vitamin A shows protective effect by regulating liver tissue Fe. We recommend to perform further investigation on the mechanisms of Vitamin A hepatoprotective mechanisms of action.