Scholarly works in Biochemistry
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Item Protocatechuic acid ameliorates neurobehavioral defìcits via suppression of H) oxidative damage, inflammation, caspase-3 and acetylcholinesterase activities in diabetic rats(Elsevier Ltd., 2019) Adedara, I. A. || || || ||; Fasina, O. B.; Ayeni, M. F.; Ajayi, O. M.; Farombi, E. O.Clinical and experimental data have demonstrated that diabetes is associated with neurological complications. Protocatechuic acid (PCA) is a phenolic phytochemical widely reported to possess antidiabetic property. However, there is no scientific information on the influence of PCA on diabetes-induced neurotoxicity. The present study aimed at investigating the neuroprotective mechanism of PCA in streptozotozin (STZ)-induced type 1 diabetic rats orally treated with PCA (50 mg/kg body weight) or glibenclamide (5 mg/kg body weight) for 45 consecutive days. Locomotor behavior was analyzed using video-tracking software during the 8-min trial in a novel environment whereas the pancreas, cerebrum and cerebellum of the rats were processed for biochemical analyses. Results showed that treatment of diabetic rats with PCA at 50 mg/kg significantly (p < 0.05) im- proved the locomotor and motor activities including the average speed, total time mobile, distance travelled, body rotation, turn angle, forelimb grip and grooming when compared with untreated diabetic rats. Moreover, the prevention of diabetes-mediated increase in acetylcholinesterase activity, biomarkers of inflammatory and oxidative stress as well as caspase 3 activity by PCA treatment was accompanied by improved pancreatic, cer- ebral and cerebellar architectures. Collectively, the neuroprotective mechanisms of PCA is related to its anti- oxidant, anti-inflammatory and anti-apoptotic activities.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 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 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.