Browsing by Author "Mustapha, O. A."

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    Protective effect of cholecalciferol against cobalt‑induced neurotoxicity in rats: ZO‑1/iFABP, ChAT/AchE and antioxidant pathways as potential therapeutic targets
    (Springer Science+Business Media, LLC, 2024) Akinrinde, A. S.; Adeoye, B. O.; Samuel, E. S.; Mustapha, O. A.
    Cobalt (Co) toxicity has been reported to produce central nervous system and gastrointestinal abnormalities. This study assessed the therapeutic effect of cholecalciferol (Cho) supplementation against damages caused by sub-acute (14-day) cobalt chloride (CoCl2) exposure in the brain and intestines. Thirty-five male Wistar rats were divided equally into five groups: Group I (control) received no treatment; Group II received oral CoCl2 (100 mg/kg) only; Groups III, IV, and V received 1000, 3000 and 6000 IU/kg of cholecalciferol, respectively by oral gavage, and concurrently with CoCl2. Cobalt-treated rats showed neuronal vacuolation and presence of pyknotic nuclei in the cerebral cortex and hippocampus, depletion of Purkinje cells in the cerebellum, as well as inflammation and congestion in the intestinal mucosa. Cobalt also increased brain and intestinal hydrogen peroxide (H2O2) and malondialdehyde (MDA) concentrations, while simultaneously reducing glutathione (GSH) content, superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione S-transferase (GST) activities. Further, CoCl2 induced increases in brain acetylcholinesterase (AchE) activity and serum zonulin (ZO-1) levels. Conversely, Cho administration suppressed CoCl2-induced damages in the brain and intestines by reducing lipid peroxidation and increasing the activities of antioxidant enzymes. Remarkably, Cho produced stimulation of brain choline acetyltransferase (ChAT) and suppression of AchE activity, along with dose-dependent reduction in serum levels of ZO-1, intestinal fatty acid-binding protein (iFABP) and nitric oxide. In conclusion, the protective role of cholecalciferol against cobalt-induced toxicity occurred via modulation of cholinergic, intestinal permeability and antioxidant pathways. The results may prove significant in the context of the role of gut-brain connections in neuroprotection.
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    Protective effect of cholecalciferol against cobalt‑induced neurotoxicity in rats: ZO‑1/iFABP, ChAT/AchE and antioxidant pathways as potential therapeutic targets
    (Springer Science+Business Media, LLC, 2024) Akinrinde, A. S.; Adeoye, B. O.; Samuel, E. S.; Mustapha, O. A.
    Cobalt (Co) toxicity has been reported to produce central nervous system and gastrointestinal abnormalities. This study assessed the therapeutic effect of cholecalciferol (Cho) supplementation against damages caused by sub-acute (14-day) cobalt chloride (CoCl2) exposure in the brain and intestines. Thirty-five male Wistar rats were divided equally into five groups: Group I (control) received no treatment; Group II received oral CoCl2 (100 mg/kg) only; Groups III, IV, and V received 1000, 3000 and 6000 IU/kg of cholecalciferol, respectively by oral gavage, and concurrently with CoCl2. Cobalt-treated rats showed neuronal vacuolation and presence of pyknotic nuclei in the cerebral cortex and hippocampus, depletion of Purkinje cells in the cerebellum, as well as inflammation and congestion in the intestinal mucosa. Cobalt also increased brain and intestinal hydrogen peroxide (H2O2) and malondialdehyde (MDA) concentrations, while simultaneously reducing glutathione (GSH) content, superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione S-transferase (GST) activities. Further, CoCl2 induced increases in brain acetylcholinesterase (AchE) activity and serum zonulin (ZO-1) levels. Conversely, Cho administration suppressed CoCl2-induced damages in the brain and intestines by reducing lipid peroxidation and increasing the activities of antioxidant enzymes. Remarkably, Cho produced stimulation of brain choline acetyltransferase (ChAT) and suppression of AchE activity, along with dose-dependent reduction in serum levels of ZO-1, intestinal fatty acid-binding protein (iFABP) and nitric oxide. In conclusion, the protective role of cholecalciferol against cobalt-induced toxicity occurred via modulation of cholinergic, intestinal permeability and antioxidant pathways. The results may prove significant in the context of the role of gut-brain connections in neuroprotection.
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    Some aspects of the orbital and ocular morphometry of the African giant rat (Cricetomys gambianus, Waterhouse)
    (African Association of Veterinary Anatomists, 2011) Olude, M. A.; Olopade, J. O.; Igado, O. O.; Mustapha, O. A.; Akinloye, A. K.
    This work was designed to investi gate some aspects of the ocular and orbital morphometric characteristics of the African giant rat (Cricetomys gambianus, Waterhouse). 16 Afri can giant rats consisting of 8 males and 8 female rats were euthanized; the eyeballs were enucleated and their skulls macerated to give 18 morphometric parameters. Student t-test and Pearson’s correlation stu dies were used to analyze the ob tained values. Correlation studies showed significance in the left orbit al height as correlated against the right orbital index. The eyeball weight for right and left eyeballs were 0.16 g and 0.15 g.The mean eyeball circumference (antero- posterior and medio-lateral) mea surements were 2.23 ± 0.01cm and 2.02 ± 0.06 cm for the left and 2.06 ± 0.04 cm and 2.13 ± 0.03 cm for the right eyeball respectively. The mean right orbital length, right orbit al height, left orbital height and the intercanthi width were 2.09 ± 0.02 cm, 1.21 ± 0.03 cm, 1.23 ± 0.03 cm and 0.93± 0.03 cm respectively but were all statistically higher (p< 0.05) in males than females exhibiting sexual dimorphism.