Environmental and occupational exposure to metal mixtures due to various geogenic and anthropogenic activities poses a health threat to exposed organisms. The outcome of systemic interactions of metals is a topical area of research because it may cause either synergistic or antagonistic effect. The present study investigated the impact of co-exposure to environmentally relevant concentrations of waterborne nickel (75 and 150 μg NiCl ₂ L⁻¹) and zinc (100 and 200 μg ZnCl₂ L⁻¹) mixtures on neurobehavioural performance of rats. Locomotor, motor and exploratory activities were evaluated using video-tracking software during trial in a novel arena and thereafter, biochemical and histological analyses were performed using the cerebrum, cerebellum and liver. Results indicated that zinc significantly (p < 0.05) abated the nickel-induced locomotor and motor deficits as well as improved the exploratory activity of exposed rats as verified by track plots and heat map analyses. Moreover, zinc mitigated nickel-mediated decrease in acetylcholinesterase activity, elevation in biomarkers of liver damage, levels of reactive oxygen and nitrogen species as well as lipid peroxidation in the exposed rats when compared with control. Additionally, nickel mediated decrease in antioxidant enzyme activities as well as the increase in tumour necrosis factor alpha, interleukin-1 beta and caspase-3 activity were markedly abrogated in the cerebrum, cerebellum and liver of rats co-exposed to nickel and zinc. Histological and histomorphometrical analyses evinced that zinc abated nickel-mediated neurohepatic degeneration as well as quantitative reduction in the widest diameter of the Purkinje cells and the densities of viable granule cell layer of dentate gyrus, pyramidal neurones of cornu ammonis 3 and cortical neurons in the exposed rats. Taken together, zinc abrogated nickel-induced neurohepatic damage via suppression of oxido-inflammatory stress and caspase-3 activation in rats.

由于各种地质和人为活动，环境和职业对金属混合物的暴露对暴露的生物构成健康威胁。金属的系统性相互作用的结果是一个热门的研究领域，因为它可能引起协同作用或拮抗作用。本研究调查了共同暴露对环境相关浓度的水性镍（75和150μgNiCl ₂  L ^-1）和锌（100和200μgZnCl ₂  L ^{-1）的影响}）混合物对大鼠神经行为的影响。在一个新的竞技场进行试验期间，使用视频跟踪软件评估了运动，运动和探索活动，此后，使用大脑，小脑和肝脏进行了生化和组织学分析。结果表明，锌显着（p <0.05）减轻了镍诱导的运动和运动功能障碍，并改善了裸露大鼠的探索活动，这已通过轨迹图和热图分析证实。此外，与对照组相比，锌可减轻镍介导的乙酰胆碱酯酶活性下降，肝损伤生物标志物升高，活性氧和氮物种水平以及脂质过氧化作用的降低。此外，共同暴露于镍和锌。组织学和组织形态计量学分析表明，锌消除了镍介导的神经肝变性，并定量减少了浦肯野细胞的最宽直径和齿状回的活性颗粒细胞层的密度，角u的锥体神经元3和皮层神经元的密度。大鼠。两者合计，锌通过抑制大鼠的氧化炎性应激和caspase-3活化消除了镍诱导的神经肝损伤。