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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 Diphenyl diselenide abrogates brain oxidative injury and neurobehavioural deficits associated with pesticide chlorpyrifos exposure in rats(Elsevier B.V., 2018) Adedara, I. A. || || || || || ||; Owoeye, O.; Awogbindin, I. O.; Ajayi, O. B.; Adeyemo, O. A.; Rocha, J. B. T.; Farombi, E. O.Exposure to pesticide chlorpyrifos (CPF) is associated with neurodevelopmental toxicity both in humans and animals. Diphenyl diselenide (DPDS) is a simple synthetic organoselenium well reported to possess antioxidant, anti-inflammatory and neuroprotective effects. However, there is paucity of information on the beneficial effects of DPDS on CPF-mediated brain injury and neurobehavioural deficits. The present study investigated the neuroprotective mechanism of DPDSin rats sub-chronically treated with CPF alone at 5 mg/kg body weight or orally co-treated with DPDS at 2.5 and 5 mg/kg body weight for 35 consecutive days. Endpoint analyses using video- tracking software in a novel environment revealed that co-treatment with DPDS significantly (p < 0.05) pro- tected against CPF-mediated locomotor and motor deficits precisely the decrease in maximum speed, total distance travelled, body rotation, absolute turn angle, forelimb grip strength as well as the increase in negative geotaxis and incidence of fecal pellets. The enhancement in the neurobehavioral activities of rats co-treated with DPDS was verified by track plot analyses. Besides, DPDS assuaged CPF-induced decrease in acetylcholinesterase and antioxidant enzymes activities and the increase in myeloperoxidase activity and lipid peroxidation level in the mid-brain, cerebral cortex and cerebellum of the rats. Histologically, DPDS co-treatment abrogated CPF- mediated neuronal degeneration in the cerebral cortex, dentate gyrus and cornu ammonis3 in the treated rats. In conclusion, the neuroprotective mechanisms of DPDS is related to the prevention of oxidative stress, enhance- ment of redox status and acetylcholinesterase activity in brain regions of the rats. DPDS may be a promising chemotherapeutic agent against brain injury resulting from CPF exposure.Item Neuroprotection of luteolin against methylmercury-induced toxicityin lobster cockroach Nauphoeta cinerea(Elsevier B.V., 2016) Adedara, I. A. || || || || ||; Rosemberg, D. B.; Souza, D. O.; Farombi, E. O.; Aschner, M.; Rocha, J. B. T.Luteolin (3_, 4_, 5, 7-tetrahydroxyflavone) is a polyphenolic compound found in foods of plant origin and has been reported to possess antioxidant and neuroprotective properties. However, there is dearth of information on the beneficial effects of luteolin on methylmercury (MeHg), a long-established neuro-toxic compound in animals and humans. This study evaluated the effect of luteolin on MeHg-inducedbehavioral and biochemical deficits, using lobster cockroach Nauphoeta cinerea as an alternative and complementary animal model. The insects were exposed for 35 consecutive days to either MeHg alone(0.05 mg/g feed) or in combination with luteolin at 0.25, 0.5 and 1.0 mg/g feed. Locomotor behavior was assessed using video-tracking software during a 10-min trial in a novel arena and subsequently, biochemical analyses were carried out using the cockroaches’ heads. Luteolin supplementation dose-dependentlyreversed the MeHg-induced locomotor deficits and enhanced the exploratory profiles of MeHg-exposedcockroaches as confirmed by track and occupancy plot analyses. Luteolin reversed the MeHg-inducedacetylcholinesterase activity inhibition, decreased dichlorofluorescein oxidation and lipid peroxidation levels, but increased total thiol level and catalase and glutathione S-transferase activities in the treated cockroaches. In conclusion, luteolin prevented oxidative stress indices and neurobehavioral deficits in a Nauphoeta cinerea model of MeHg toxicity.Item Influence of diphenyl diselenide on chlorpyrifos-induced toxicity in Drosophila melanogaster(Elsevier GmbH., 2015) Adedara, I. A.; Klimaczewski, C. V.; Barbosa, N. B. V.; Farombi, E. O.; Souza, D. O.; Rocha, J. B. T.Exposure to chlorpyrifos (CPF) poses several harmful effects to human and animal health. The present study investigated the influence of diphenyl diselenide (DPDS) on CPF-induced toxicity in Drosophila melanogaster. Firstly, the cumulative responses of virgin flies (2- to 3-day-old) to CPF (0.075–0.6 µg/g) and DPDP (5–40 µmol/kg) in the diet for 28 consecutive days were investigated. Subsequently, the protective effect of DPDS (10, 20 and 40 µmol/kg) on CPF (0.15 µg/g)-induced mortality, locomotor deficits, neurotoxicity and oxidative stress was assessed in a co-exposure paradigm for 7 days. Results showed that CPF exposure significantly decreased the operant reflex in a time- and concentration-dependent manner, whereas the percent live flies with DPDS treatment was not statistically different from control following 28 days of treatment. In the co-exposure study, CPF significantly increased mortality while the survivors exhibited significant locomotor deficits with decreased acetylcholinesterase (AChE) activity. Dietary supplementation with DPDS was associated with marked decrease in mortality, improvement in locomotor activity and restoration of AChE activity in CPF-exposed flies. Moreover, CPF exposure significantly decreased catalase and glutathione-S-transferase activities, total thiol level with concomitant significant elevation in levels of reactive oxygen species and thiobarbituric acid reactive substances in the head and body regions of the treated flies. Dietary supplementation with DPDS significantly improved the antioxidant status and prevented CPF-induced oxidative stress, thus demonstrating the protective effect of DPDS in CPF-treated flies.