Zinc or/and Vitamin E Supplementation Mitigates Oxidative Stress, Neuroinflammation, Neurochemical Changes and Behavioural Deficits in Male Wistar Rats Exposed to Bonny Light Crude Oil.

Background: Crude oil, a major key economic driver in developing countries, is also of environmental concern, linked to neurotoxicity and behavioural problems. Despite the known neurotoxic effects of crude oil and the potential benefits of zinc and vitamin E, there is a paucity of research specifically addressing their combined efficacy in mitigating neurochemical changes and behavioural deficits induced by crude oil. Current studies have largely focussed on the individual effects of these supplements in different contexts, but their synergistic potential in a crude oil exposure model remains underexplored. This study investigated the potential effects of zinc and vitamin E on neurobehavioural alterations in male Wistar rats fed with Bonny light crude oil (BLCO)-contaminated diet. Methods: Thirty (30) male Wistar rats (160 ± 10 g) were assigned into five groups (n = 6). Group 1 received standard rat feed, Group 2 was exposed to BLCO (0.1 mL/g of rat feed) for 3 weeks, and groups 3-5 were treated with zinc (50 mg/kg/day), vitamin E (400 IU/kg), or both [vitamin E (400 IU/kg) + zinc (50 mg/kg/day)], respectively for 1 week after BLCO exposure for 3 weeks. Locomotive, anxiolytic, depressive-like behaviours and spatial memory were assessed using the open-field test, elevated plus maze, forced swim test and Y-maze. Rats were sacrificed and the brain samples were collected for biochemical assays at the end of the behavioural tests. Results: Zinc and vitamin E supplementation (individually or combined) significantly increased brain total antioxidant capacity and superoxide dismutase (SOD) activity, reduced inflammatory markers (TNF-alpha) and lipid peroxidation, normalized neurotransmitter levels in the brain and improved behavioural performance. Conclusion: Treatment with Zn and/or vitamin E reverses BLCO-induced neurobehavioural alterations via modulation of oxidative stress, inflammation and neurotransmitters.