EFFECT OF SELENIUM SUPPLEMENTATION ON CATALASE AND GLUTATHIONE-S-TRANSFERASE IN ACETAMINOPHEN-INDUCED TOXICITY IN WISTAR RATS

Acetaminophen (paracetamol) is a widely used analgesic and antipyretic drug. Although it is considered safe at therapeutic doses, overdose or prolonged exposure may lead to severe oxidative stress and organ toxicity, particularly in the liver and kidneys. The toxicity is primarily mediated through the formation of a reactive metabolite known as N-acetyl-p-benzoquinone imine (NAPQI), which depletes endogenous antioxidant defenses and promotes oxidative damage. Antioxidant enzymes such as catalase and glutathione-S-transferase play vital roles in protecting cells from oxidative injury by detoxifying reactive oxygen species and harmful metabolites. Selenium is an essential trace element known for its strong antioxidant properties and its role in regulating several antioxidant enzymes. The present study investigates the effect of selenium supplementation on catalase and glutathione-S-transferase activities in acetaminophen-induced toxicity in Wistar rats. Experimental animals were divided into control and treatment groups, with toxicity induced using acetaminophen while selenium supplementation was administered to evaluate its protective effects. The results indicated that acetaminophen administration significantly reduced the activities of catalase and glutathione-S-transferase due to oxidative stress. However, selenium supplementation restored and significantly increased the activities of these antioxidant enzymes compared with untreated toxic groups. These findings suggest that selenium supplementation may exert protective effects against acetaminophen-induced oxidative damage by enhancing antioxidant defense mechanisms. The study concludes that selenium ”osse’ses significant antioxidant potential and may be useful in reducing drug-induced oxidative toxicity. Further studies are recommended to explore its therapeutic applications in clinical toxicology.