ArticlePsychopharmacology2022
Selenium abates manganese-induced striatal and hippocampal toxicity via abrogation of neurobehavioral deficits, biometal accumulation, oxidative stress, inflammation, and caspase-3 activation in rats.
Article in Psychopharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 18 citations in OpenAlex.
- Rice bran extract ameliorates metal mixture induced cerebral cortex dysfunction: implicating the Nrf-2/HMOX-1/BDNF signalling pathway.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026Article
- Manganese Exposure Is Associated with Reduced Grip Strength: Evidence from Humans and Mice.Toxics · 2025Article
- Combined Restraint Stress and Metal Exposure Paradigms in Rats: Unravelling Behavioural and Neurochemical Perturbations.Molecular neurobiology · 2025Article
- Associations between Metals, Serum Folate, and Cognitive Function in the Elderly: Mixture and Mediation Analyses.Environment & health (Washington, D.C.) · 2024Article
- Scientific opinion on the tolerable upper intake level for manganese.EFSA journal. European Food Safety Authority · 2023Article
- Metallothionein-2A Protects Cardiomyocytes from Hypoxia/reper-Fusion through Inhibiting p38.Cell biochemistry and biophysics · 2023Article
- Sex-dependent metal accumulation and immunoexpression of Hsp70 and Nrf2 in rats' brain following manganese exposure.Environmental toxicology · 2022Article
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Excessive exposure to manganese (Mn) is associated with neurotoxicity characterized by oxidative stress, inflammation, and apoptosis induction. Selenium (Se) has been shown to possess antioxidant, anti-inflammatory, and anti-apoptotic properties in humans and animals. The present study investigated the neuroprotective mechanism of Se in rats sub-chronically treated with Mn at 30 mg/kg body weight or orally co-treated with Se at 0.2 and 0.4 mg/kg body weight for 35 consecutive days. Locomotive and exploratory profiles were recorded and computed with the aid of ANY-Maze (a video-tracking software) for 5-min trial, in a novel apparatus. The ANY-Maze analysis showed that Se significantly (p < 0.05) abated Mn-induced locomotive impairment evidenced by increased in maximum speed, total time traveled, absolute turn angle, number of line crossing, rotation and forelimb grip and decreased total time immobile, grooming, and negative geotaxis as verified by the enhanced track plot density. Furthermore, the striatum and hippocampus of the rats were excised and the levels of Mn and Se, oxidative stress markers, proinflammatory cytokines including acetylcholinesterase and caspase-3 activities were assayed. The result shows that Se abates Mn-mediated accumulation of Mn. Also, Se ameliorated Mn-induced decrease in antioxidant enzymes as well as glutathione level and increase in acetylcholinesterase activity, lipid peroxidation, proinflammatory cytokines (i.e., interleukin (IL)-6, IL-1β, tumor necrosis factor alpha), and caspase-3 activation in the striatum and hippocampus of the rats. Collectively, Se abated Mn-induced striatal and hippocampal toxicity via abrogation of neurobehavioral deficits, biometal accumulation, oxidative stress, inflammation, and caspase-3 activation in rats. Se may serve as a neuroprotective agent against Mn-mediated neurotoxicity.
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