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Item Kolaviron via anti-inflammatory and redox regulatory mechanisms abates multi-walled carbon nanotubes-induced neurobehavioral deficits in rats(Springer-Verlag GmbH, 2020) Adedara, I. A.; Awogbindin, I. O.; Owoeye, O.; Maduako, I. C.; Ajeleti, A. O.; Owumi, S. E.; Patlola, A. K.; Farombi, E. O.Exposure to multi-walled carbon nanotubes (MWCNTs) reportedly elicits neurotoxic effects. Kolaviron is a phytochem- ical with several pharmacological effects namely anti-oxidant, anti-inflammatory, and anti-genotoxic activities. The present study evaluated the neuroprotective mechanism of kolaviron in rats intraperitoneally injected with MWCNTs alone at 1 mg/kg body weight or orally co-administered with kolaviron at 50 and 100 mg/kg body weight for 15 consecutive days. Following exposure, neurobehavioral analysis using video-tracking software during trial in a novel environment indicated that co-administration of both doses of kolaviron significantly (p < 0.05) enhanced the locomotor, motor, and exploratory activities namely total distance traveled, maximum speed, total time mobile, mobile episode, path efficiency, body rotation, absolute turn angle, and negative geotaxis when compared with rats exposed to MWCNTs alone. Further, kolaviron markedly abated the decrease in the acetylcholinesterase activity and antioxidant defense system as well as the increase in oxidative stress and inflammatory biomarkers induced by MWCNT exposure in the cerebrum, cerebellum, and mid-brain of rats. The amelioration of MWCNT-induced neuronal degeneration in the brain structures by kolaviron was verified by histological and morphometrical analyses. Taken together, kolaviron abated MWCNT-induced neurotoxicity via anti-inflammatory and redox regulatory mechanisms.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 Neuroprotective influence of taurine on fluoride-induced biochemical and behavioral deficits in rats(Elsevier Ireland Ltd., 2017) Adedara, I. A.; Abolaji, A. O.; Idris, U. F.; Olabiyi, B. F.; Onibiyo, E. M.; Ojuade, T. D.; Farombi, E. O.Epidemiological and experimental studies have demonstrated that excessive exposure to fluoride induced neurodevelopmental toxicity both in humans and animals. Taurine is a free intracellular b- amino acid with antioxidant and neuroprotective properties. The present study investigated the neu- roprotective mechanism of taurine by evaluating the biochemical and behavioral characteristics in rats exposed to sodium fluoride (NaF) singly in drinking water at 15 mg/L alone or orally co-administered by gavage with taurine at 100 and 200 mg/kg body weight for 45 consecutive days. Locomotor behavior was assessed using video-tracking software during a 10-min trial in a novel environment while the brain structures namely the hypothalamus, cerebrum and cerebellum of the rats were processed for biochemical determinations. Results showed that taurine administration prevented NaF-induced loco- motor and motor deficits namely decrease in total distance travelled, total body rotation, maximum speed, absolute turn angle along with weak forelimb grip, increased incidence of fecal pellets and time of grooming, immobility and negative geotaxis. The taurine mediated enhancement of the exploratory profiles of NaF-exposed rats was supported by track and occupancy plot analyses. Moreover, taurine prevented NaF-induced increase in hydrogen peroxide and lipid peroxidation levels but increased acetylcholinesterase and the antioxidant enzymes activities in the hypothalamus, cerebrum and cere- bellum of the rats. Collectively, taurine protected against NaF-induced neurotoxicity via mechanisms involving the restoration of acetylcholinesterase activity and antioxidant status with concomitant inhi- bition of lipid peroxidation in the brain of rats.Item Quercetin improves neurobehavioral performance through restoration of brain antioxidant status and Acetylcholinesterase activity in Manganese-treated rats(Springer Science+Business Media, 2017) Adedara, I. A.; Ego, V. C.; Subair, T. I.; Oyediran, O.; Farombi, E. O.The present study investigated the neuroprotective mechanism of quercetin by assessing the biochemical and behavioral characteristics in rats sub-chronically treated with manganese alone at 15 mg/kg body weight or orally co-treated with quercetin at 10 and 20 mg/kg body weight for 45 consecutive days. Locomotor behavior was monitored using video-tracking software during a 10-min trial in a novel environment whereas the brain regions namely the hypothalamus, cerebrum and cerebellum of the rats were processed for biochemical analyses. Results indicated that co-treatment with quercetin significantly (p < 0.05) prevented manganese-induced locomotor and motor deficits specifically the decrease in total distance travelled, total body rotation, maximum speed, absolute turn angle as well as the increase in time of immobility and grooming. The improvement in the neurobehavioral performance of manganese-treated rats following quercetin co-treatment was confirmed by track and occupancy plot analyses. Moreover, quercetin assuaged manganese-induced decrease in antioxidant enzymes activities and the increase in acetylcholinesterase activity, hydrogen peroxide generation and lipid peroxidation levels in the hypothalamus, cerebrum and cerebellum of the rats. Taken together, quercetin mechanisms of ameliorating manganese-induced neurotoxicity is associated with restoration of acetylcholinesterase activity, augmentation of redox status and inhibition of lipid peroxidation in brain of rats.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.