EFFECT OF SELENIUM SUPPLEMENTATIOM ON TOTAL ANTIOXIDANT CAPACITY AND MALONDIADEHYDE IN ACETAMINOPHEN-INDUCED TOXICITY IN WISTAR RATS

Acetaminophen overdose is a common cause of drug-induced liver toxicity, largely due to the generation of reactive oxygen species (ROS) and oxidative stress. Selenium, an essential trace element with potent antioxidant properties, plays a crucial role in activating glutathione peroxidase, a key enzyme in the detoxification of ROS. This study investigates the effect of selenium on total antioxidant capacity (TAC) and malondialdehyde (MDA) levels, a marker of lipid peroxidation, in Wistar rats subjected to acetaminophen-induced toxicity. 20 Wistar rats were divided into four groups. Group 1: (Control group) received normal rat chow and water only, Group 2: (Acetaminophen only) received 0.2mls of 7grams of acetaminophen, Group 3: (Selenium only) received 0.2mls of 7g of selenium and Group 4: (Selenium and Acetaminophen) received 0.2mls of 7g of selenium and 0.2mls of 7grams of acetaminophen. The administration lasted for 21 days and rats were sacrificed and the blood was collected and assayed for TAC activity and MDA activity. Acetaminophen administration resulted in a significant increase in TAC and an decrease in MDA levels, indicating oxidative stress and lipid peroxidation. Selenium supplementation significantly increase TAC and reduced MDA levels in the selenium + acetaminophen-treated group compared to other group. These findings suggest that selenium supplementation exerts a protective effect by enhancing the antioxidant defense system and reducing oxidative damage in acetaminophen-induced toxicity. The results highlight selenium’s potential as a therapeutic agent in managing drug-induced oxidative stress. Further studies are required to elucidate the mechanisms and optimal dosing for selenium’s protective effects in such toxicological conditions.