Ogunmiluyi Oluwafunmbi Ebenezer, Naiho Alexander Obidike, Emojevwe Victor Oghenekparobo, Oladele Tolulope Samuel, Adebisi Kayode Adedoyin, Siyanbade Jacob Adewale, Akinola Adeniran Oluwadamilare
Department of Physiology, University of Medical Sciences, Ondo, Ondo, Nigeria.
Department of Physiology, University of Delta, Agbor, Delta, Nigeria.
J Toxicol. 2024 Dec 21;2024:9317271. doi: 10.1155/jt/9317271. eCollection 2024.
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. Thirty (30) male Wistar rats (160 ± 10 g) were assigned into five groups ( = 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. 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. Treatment with Zn and/or vitamin E reverses BLCO-induced neurobehavioural alterations via modulation of oxidative stress, inflammation and neurotransmitters.
原油是发展中国家主要的关键经济驱动力，但也引发了环境问题，与神经毒性和行为问题相关。尽管原油具有已知的神经毒性作用，以及锌和维生素E的潜在益处，但专门研究它们在减轻原油诱导的神经化学变化和行为缺陷方面联合功效的研究却很匮乏。目前的研究主要集中在这些补充剂在不同情况下的个体作用，但它们在原油暴露模型中的协同潜力仍未得到充分探索。本研究调查了锌和维生素E对喂食受邦尼轻质原油（BLCO）污染饲料的雄性Wistar大鼠神经行为改变的潜在影响。将30只雄性Wistar大鼠（体重160±10克）分为五组（每组n = 6）。第1组给予标准大鼠饲料，第2组暴露于BLCO（0.1毫升/克大鼠饲料）3周，第3 - 5组在暴露于BLCO 3周后分别用锌（50毫克/千克/天）、维生素E（400国际单位/千克）或两者[维生素E（400国际单位/千克）+锌（50毫克/千克/天）]治疗1周。使用旷场试验、高架十字迷宫、强迫游泳试验和Y迷宫评估运动、抗焦虑、抑郁样行为和空间记忆。行为测试结束时处死大鼠并收集脑样本进行生化分析。补充锌和维生素E（单独或联合）显著提高了大脑总抗氧化能力和超氧化物歧化酶（SOD）活性，降低了炎症标志物（肿瘤坏死因子-α）和脂质过氧化，使大脑中的神经递质水平恢复正常并改善了行为表现。用锌和/或维生素E治疗通过调节氧化应激、炎症和神经递质逆转了BLCO诱导的神经行为改变。
