AI Article Synopsis
- Manganese is essential for biological functions but excessive levels can cause manganism, a neurological disorder.
- A study was conducted on rats to evaluate the toxic effects of manganese exposure by analyzing weight, motor skills, and biochemical changes in brain mitochondria.
- The results showed that manganese exposure led to weight loss and impaired motor function, while edaravone treatment suggested a protective effect against manganese-induced damage.
Article Abstract
Manganese (Mn) is a required element for biological systems; however, its excessive exposure may lead to a neurological syndrome known as manganism. The aim of the present study was to assess the toxic effects of subacute exposure of Mn by measuring weight gain, motor performance, and biochemical parameters (complex I activity, lipid peroxides, and protein carbonyls) in brain mitochondria in rats. We also examined whether edaravone (EDA), a radical scavenger, exerts protective effects against Mn-induced neurotoxicity. In addition, we evaluated the accumulation of Mn in brain regions using magnetic resonance imaging. Mn-exposed rats revealed significantly impaired motor performance, weight loss, and Mn accumulation in particular brain area. Lipid peroxides and protein carbonyls were significantly increased in Mn-exposed rats, whereas complex I activity was found to be decreased. EDA treatment significantly prevented mitochondrial oxidative damage and improved motor performance. These findings suggested that EDA might serve as a clinically effective agent against Mn-induced neurotoxicity.
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| http://dx.doi.org/10.1002/jbt.21780 | DOI Listing |
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