Probucol neuroprotection against manganese-induced damage in adult Wistar rat brain slices.
Sarah Camboim Del Rio NaizKarina Giacomini VarelaDiego de CarvalhoAline Pertile RemorPublished in: Toxicology and industrial health (2023)
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 (MnCl 2 ) 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.
Keyphrases
- oxidative stress
- diabetic rats
- cerebral ischemia
- anti inflammatory
- cell death
- dna damage
- subarachnoid hemorrhage
- induced apoptosis
- ischemia reperfusion injury
- room temperature
- high glucose
- metal organic framework
- functional connectivity
- transition metal
- blood brain barrier
- brain injury
- resting state
- oxide nanoparticles
- white matter
- cell proliferation
- heat shock
- smoking cessation
- signaling pathway
- cerebral blood flow
- heat shock protein