Probucol neuroprotection against manganese-induced damage in adult Wistar rat brain slices

Author:

Del Rio Naiz Sarah Camboim1,Varela Karina Giacomini2,de Carvalho Diego2ORCID,Remor Aline Pertile2ORCID

Affiliation:

1. Graduação em Medicina, Universidade do Oeste de Santa Catarina (UNOESC), Joaçaba, Brazil

2. Programa de Pós-Graduação em Biociências e Saúde (PPGBS), Área de Ciências da Vida e Saúde, Universidade do Oeste de Santa Catarina (UNOESC), Joaçaba, Brazil

Abstract

Manganese (Mn) is an abundant element used for commercial purposes and is essential for the proper function of biological systems. Chronic exposure to high Mn concentrations causes Manganism, a Parkinson's-like neurological disorder. The pathophysiological mechanism of Manganism remains unknown; however, it involves mitochondrial dysfunction and oxidative stress. This study assessed the neuroprotective effect of probucol, a hypolipidemic agent with anti-inflammatory and antioxidant properties, on cell viability and oxidative stress in slices of the cerebral cortex and striatum from adult male Wistar rats. Brain structure slices were kept separately and incubated with manganese chloride (MnCl2) and probucol to evaluate the cell viability and oxidative parameters. Probucol prevented Mn toxicity in the cerebral cortex and striatum, as evidenced by the preservation of cell viability observed with probucol (10 and 30 μM) pre-treatment, as well as the prevention of mitochondrial complex I inhibition in the striatum (30 μM). These findings support the protective antioxidant action of probucol, attributed to its ability to prevent cell death and mitigate Mn-induced mitochondrial dysfunction.

Publisher

SAGE Publications

Subject

Health, Toxicology and Mutagenesis,Public Health, Environmental and Occupational Health,Toxicology

Cited by 1 articles. 订阅此论文施引文献 订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献

1. Signal Transduction Associated with Mn-induced Neurological Dysfunction;Biological Trace Element Research;2023-12-29

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