Paraquat is a common and effective herbicide; although its poisoning could lead to severe oxidative organ damages and its main target organs are the lungs, kidneys, heart, and liver. Thymoquinone is the active ingredient of Nigella sativa which is traditionally used in herbal medicine; recent studies have shown that thymoquinone could inhibit oxidative stress. This study explores protective effects of thymoquinone on paraquat-induced hepatotoxicity in mice. Accordingly, adult male mice were randomly divided into nine groups for three continuous days intraperitoneal injection treatment: (1) control; (2) solvent; (3) 20 mg/kg vitamin E; (4) 20 mg/kg thymoquinone; (5) 20 mg/kg paraquat and Groups 6, 7, 8, and 9 received 20 mg/kg of vitamin E and 5, 10, and 20 mg/kg of thymoquinone, respectively. The last four groups, received 20 mg/kg paraquat just 24 h after pretreatments. We assessed serum liver enzymes activities, liver histopathology changes, oxidative (lipid peroxidation) and antioxidative (ferric reducing antioxidant power) potential, superoxide dismutase (SOD) and catalase activity, and total thiol groups content after administration of the poison and treatments. Pretreatment with 10 mg/kg thymoquinone inhibited, safely, the elevations in levels of liver function tests (LFTs) and lipid peroxidation, restored the activity of SOD, and ameliorated the histopathological alterations induced by paraquat. Eventually, our results indicate that thymoquinone performs its hepatoprotective role in mice by prevention of SOD suppression mediated by paraquat.
Keywords: Liver; Mice; Oxidative damage; Paraquat; SOD; Thymoquinone.
Copyright © 2018. Published by Elsevier Inc.