Advances in Research

Ferulic acid (FA) is a dietary phytochemical formed during the metabolism of phenylalanine and tyrosine. Disruption of mitochondria and free radical mediated tissue injury has been reported during liver toxicity induced by carbon tetrachloride, potent hepatotoxic agent. The present study was designed to investigate the antioxidant protective effect of ferulic acid on hepatocytes, liver function and mitochondrial electron respiratory chain enzymes in hepatotoxic rats. Rats were classified into four groups : normal control group, hepatotoxic group subcutaneously injected with CCl4  once weekly for 4 weeks; third group: hepatotoxic group daily administered orally FA with a dose of 20 mg/Kg b.wt., and forth group: hepatotoxic group daily administered orally FA with a dose of 80 mg/Kg b.wt. The model of CCl₄-injected hepatocellular rats elicited declines in liver antioxidant enzyme activities; glutathione peroxidase, superoxide dismutase , Catalase in association of a reduction in reduced glutathione, serum total protein with concomitant significant elevations in lipid peroxidation marker , serum nitric oxide,and liver enzymes,  lactate dehydrogenase and total bilirubin. CCl₄ resulted in a significant decrease in the activities of mitochondrial respiratory chain enzymes (NADH dehydrogenase and cytochrome c oxidase). FA enhanced the attenuation of these functional abnormalities and restored normal mitochondrial function when compared to rats CCl₄ toxicant treated groups , the attenuating effect was more pronounced in FA low dose Hence, these findings demonstrate the ameliorative role of FA on mitochondrial function during CCl₄ induced hepatotoxicity and associated oxidative stress in rats.