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African Journal of Biomedical Research
Ibadan Biomedical Communications Group
ISSN: 1119-5096
Vol. 11, No. 2, 2008, pp. 183-190
Bioline Code: md08024
Full paper language: English
Document type: Research Article
Document available free of charge

African Journal of Biomedical Research, Vol. 11, No. 2, 2008, pp. 183-190

 en Protective Effect of Oral Ascorbic Acid (Vitamin C) Against Acetaminophen-Induced Hepatic Injury in Rats
Adeneye, Adejuwon A. & Olagunju, Joseph O.


The incidence of acetaminophen-induced hepatotoxicity is reported to be on the increase, with limited therapeutic or chemoprophylactic options. In the present in vivo study, single daily oral doses (100 - 500 mg/kg) of ascorbic acid (ASC) were investigated for their protective effects against acetaminophen (APAP)-induced hepatotoxicity in 4 groups of rats made up of 6 rats per group for 14 days. Also, effects of the doses on body weights taken on the 1st, 7th and 15th day of the experiment were also investigated. On the 15th day, blood samples for serum ALT, AST and FBG assay were collected through cardiac puncture under inhaled diethyl ether anaesthesia. Rat livers were also studied for histopathology. Results showed that treatment with APAP intraperitoneal injection induced significant (P<0.001) elevation in the serum levels of ALT and AST while inducing significant (P<0.05) decrease in the serum FBG. The hepatotoxicity was also corroborated by the histopathological lesion of lipid peroxidation characterized by diffuse ballooning degeneration with lymphocytic infiltration. Significant (P<0.01) weight loss and hypoglycaemia were also associated with APAP-induced hepatotoxicity. However, these alterations were attenuated in ASC pretreated rats dose dependently. Also, APAP-induced hypoglycaemia and weight loss were significantly (P<0.01, P<0.001) enhanced by ASC in dose related pattern. Thus, results of this study showed that 100 - 500 mg/kg/day was protective against APAP-induced hepatotoxicity, effect which could have been mediated via its inherent free radical scavenging and/or free radicals generation inhibiting activities.

Acetaminophen-induced hepatotoxicity; Serum aminotransferases; Fasting blood glucose; Histopathology; Rats

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