Antioxidant Potentials of L-Ascorbic Acid (L-AA) and Butylated Hydroxytoluene (BHT) in CCl4-Induced Oxidative Damage of Soft Tissues in Wistar Rats

摘要

The antioxidant potentials of Butylated hydroxytoluene (BHT) and L-Ascorbic acid (L-AA) in CCl4-induced tissue damage were compared in adult female Wistar rats. Toxicity was induced in the animals via a single dose (i.p) of 20% 2 mL/Kg body weight (BW) of CCl4. BHT and L-ascorbic acid, each at a dose of 100 mg/kg BW were orally administered (twice daily for 7 days) to different groups of CCl4-treated animals. Biochemical analyses were carried out on the supernatant fractions of the liver and kidney homogenates to estimate the levels of tissue protein and malondialdehyde (MDA) as well as the activities of antioxidant enzymes: gluthatione s-transferase (GST), superoxide dismutase (SOD), and catalase (CAT). The data obtained showed that the evaluated antioxidants (BHT and L-ascorbic acid) elicited notable ameliorative effects against CCl4-induced tissue damage. Comparatively, BHT elicited relative higher catalase activity and decreased MDA concentration in CCl4-induced liver and kidney damage in rats. BHT also produced significantly higher protective effect in terms of SOD activity in the kidney of rats. Conversely, L-Ascorbic acid showed a relative higher GST and SOD activities in CCl4 induced liver damage alone. There was no significant difference in the effect of the two antioxidants on the activity of GST in the kidney. Overall, the data of this study appear to score BHT (a synthetic antioxidant) relatively higher than ascorbic acid (a natural antioxidant) in terms of in vivo antioxidant capacities within the limit of the parameters assessed. It also demonstrates that BHT elicits its antioxidant potential against CCl4 induced reactive species mainly through promotion of catalase activity and inhibition of lipid peroxidation whereas ascorbic acid maximizes its antioxidant effects against the same toxicant by promoting GST and SOD activities particularly in the liver.