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Item Neurobehavioural and biochemical responses associated with exposure to binary waterborne mixtures of zinc and nickel in rats(1382-6689, 2020) Adedara, I. A.; Adegbosin, A. N.; Owoeye, O.; Abiola, M. A.; Odunewu, A. A.; Owoeye, O.; Owumi, S. E.; Farombi, E. O.Environmental and occupational exposure to metal mixtures due to various geogenic and anthropogenic ac- tivities 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 pg NiCl 2L-1) and zinc (100 and 200pg ZnC^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 histomorphome- trical analyses evinced that zinc abated nickel-mediated neurohepatic degeneration as well as quantitative re- duction 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.Item Neuroprotective mechanisms of selenium against arsenic-induced behavioral impairments in rats(Elsevier B.V., 2020) Adedara, I. A.; Fabunmi, A. T.; Ayenitaju, A. C.; Atanda, O. E.; Adebowale, A. A.; Ajayi, B. O.; Rocha, J. B. T.; Owoeye, O.; Farombi, E. O.Environmental pollution due to arsenic is associated with several adverse health effects including neurotoxicity in animals and humans. Selenium is a nutritionally essential trace metalloid well documented to elicit com- pelling pharmacological activities in vitro and in vivo. Report on the influence of selenium on arsenic-mediated behavioral derangement is lacking in literature. Hence, to fill this knowledge gap, rats were either exposed to arsenic per se in drinking water at 60 pg AsO2Na/L or co-administered with inorganic selenium at 0.25 mg/kg or organic selenium diphenyl diselenide (DPDS) at 2.5 mg/kg body weight for 45 successive days. Neurobehavioural data from rats in a new environment using video-tracking software evinced that inorganic and organic forms of selenium significantly (p < 0.05) abrogated arsenic-induced motor and locomotor in- sufficiencies such as increased negative geotaxis and fecal pellets numbers as well as the diminution in grip strength, body rotation, maximum speed, absolute turn angle and total distance travelled. The augmentation in the behavioral activities in rats co-administered with arsenic and both forms of selenium was substantiated using track and occupancy plots analyses. Selenium mitigated arsenic-induced decreases in glutathione level and acetylcholinesterase activity as well as the increase in oxidative stress and reactive oxygen and nitrogen species. Moreover, selenium diminished inflammatory parameters (myeloperoxidase activity, nitric oxide, tumour ne- crosis factor alpha and interleukin-1 beta levels), caspase-3 activity and ameliorated histological lesions in the cerebellum, cerebrum and liver of the rats. Collectively, selenium abated arsenic-induced behavioral derange- ments via anti-inflammation, antioxidant and anti-apoptotic mechanisms in rats.Item Impact of binary waterborne mixtures of nickel and zinc on hypothalamic-pituitary-testicular axis in rats(Elsevier Ltd., 2019) Adedara, I. A.; Abiola, M. A.; Adegbosin, A. N.; Odunewu, A. A.; Farombi, E. O.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 mg NiCl2 L-1) and zinc (100 and 200 mg 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 per- oxidation 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 dysfunctionItem Selenium abates reproductive dysfunction via attenuation of biometal accumulation, oxido-inflammatory stress and caspase-3 activation in male rats exposed to arsenic(Elsevier Ltd., 2019) Adedara, I. A.; Adebowale, A. A.; Atanda, O. E.; Fabunmi, A. T.; Ayenitaju, A. C.; Rocha, J. B. T.; Farombi, E. O.Frequent exposure to arsenic is well documented to impair reproductive function in humans and animals. Biological significance of inorganic selenium and organoselenium, diphenyl selenide (DPDS), has been attributed to their pharmacological activities. However, their roles in arsenic-mediated reproductive toxicity is lacking in literature. The present study evaluated the protective effects elicited by selenium and DPDS in arsenic-induced reproductive deficits in rats. Animals were either exposed to arsenic alone in drinking water at 60 µg AsO₂Na L⁻¹ or co-treated with selenium at 0.25 mg kg⁻¹ or DPDS at 2.5 mg kg⁻¹ body weight for 45 consecutive days. Results indicated that arsenic-mediated deficits in spermatogenic indices and marker enzymes of testicular function were significantly abrogated in rats co-treated with selenium or DPDS. Additionally, selenium or DPDS co-treatment prevented arsenic-mediated elevation in oxidative stress indices and significantly suppressed arsenic-mediated inflammation evidenced by diminished myeloperoxidase activity, nitric oxide, tumor necrosis factor alpha, interleukin-1 beta levels in hypothalamus, testes and epididymis of the rats. Moreover, selenium or DPDS abrogated arsenic mediated activation of caspase-3 activity and histological lesions in the treated rats. Taken together, selenium or DPDS improved reproductive function in arsenic-exposed rats via suppression of inflammation, oxidative stress and caspase-3 activation in rats.