Neurobehavioural and biochemical responses associated with exposure to binary waterborne mixtures of zinc and nickel in rats.

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.

Impact of binary waterborne mixtures of nickel and zinc on hypothalamic-pituitary-testicular axis in rats.

Several evidences from the literature showed that the coexistence of nickel and zinc in polluted waters is related to the similarity in their geogenic and anthropogenic factors. Although most environmental exposures to metals do not occur singly, there is a paucity of scientific knowledge on the effects of zinc and nickel co-exposure on mammalian reproductive health. The present study investigated the influence of co-exposure to nickel and zinc on male reproductive function in rats. Experimental rats were co-exposed to environmentally relevant concentrations of waterborne nickel (75 and 150 µg NiCl2 L-1) and zinc (100 and 200 µg ZnCl2 L-1) for 45 successive days. Subsequently, reproductive hormones were assayed whereas the hypothalamus, epididymis and testes of the rats were processed for the assessment of oxidative stress and inflammation indices, caspase-3 activity and histology. Results indicated that co-exposure to nickel and zinc significantly (p < 0.05) abolished nickel-mediated diminution of antioxidant defense mechanisms while diminishing levels of reactive oxygen and nitrogen species and lipid peroxidation in the hypothalamus, epididymis and testes of the exposed rats. Additionally, co-exposure to zinc abated nickel-mediated diminutions in luteinizing hormone, follicle-stimulating hormone, serum and intra-testicular testosterone with concomitant enhancement of sperm production and quality. Further, zinc abrogated nickel-mediated elevation in inflammatory biomarkers including nitric oxide, tumor necrosis factor alpha, interleukin-1 beta as well as caspase-3 activity. The protective influence of zinc on nicked-induced reproductive toxicity was well supported by histological data. Overall, zinc ameliorated nickel-induced reproductive dysfunction via its anti-oxidant, anti-inflammatory, anti-apoptotic and spermato-protective activities in rats.