Browsing by Author "Noah A. Omeiza1"

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    Melatonin salvages lead-induced neuro-cognitive shutdown, anxiety, and depressive-like symptoms via oxido-inflammatory and cholinergic mechanisms
    (Brain and Behavior published by Wiley Periodicals LLC, 2021-05-19) Noah A. Omeiza1; Abdulrahim A. Halimat; Abdullateef I. Alagbonsi; Precious U. Ezurike; Talha K. Soluoku; Happy Isiabor; Abdulmusawwir A.; Alli oluwafuyi
    Abstract Introduction: Lead is the most used nonphysiological neurotoxic heavy metal in the world that has been indicated to interfere with the cognitive and noncognitive pro- cesses via numerous mechanisms. The neuroprotective effect of melatonin is well known, but the effect of its interaction with lead in the brain remains inconclusive. Objective: To assess the therapeutic role of melatonin on cognitive deficit, anxiety and depressive-like symptoms in matured male Wistar rats exposed to a subchronic lead chloride (PbCl2). Methods: Twenty male Wistar rats were blindly randomized into four groups (n = 5/group): group 1 to 4 underwent intragastric administration of physiological saline (10 ml/kg; vehicle), PbCl2 (50 mg/kg), melatonin (10 mg/kg) and PbCl2 + mela- tonin respectively for a period of 4 weeks during which neurobehavioral data were extracted, followed by neurochemical and histopathological evaluations. Results: Exposure to PbCl2 reduced cognitive performance by increasing the escape latency and average proximity to the platform zone border, decreasing average path length in the platform zone, cognitive score, and time spent in probing. It raised the thigmotaxis percentage, time spent in rearing, number of pellet-like feces, and time spent in the dark compartment of a bright/dark box which are predictors of anxiety. It also induced depressive-like behavior as immobility time was enhanced. PbCl2 deranged neurochemicals; malondialdehyde, interlukin-1β, and tumor necrotic factor-α were increased while superoxide dismutase and acetylcholinesterase were decreased without remarkable alteration in reduced glutathione and nitric oxide. Administration of PbCl2 further disrupted neuronal settings of hippocampal proper and dentate gyrus. In contrast, the supplementation of melatonin reversed all the neu- rological consequences of PbCl2 neurotoxicity by eliciting its properties against oxida- tive and nonoxidative action of PbCl2.