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Functional Neuroimaging Using Ultrasonic Blood-brain Barrier Disruption and Manganese-enhanced MRI
Published on: July 12, 2012
Protection by Edaravone, a Radical Scavenger, against Manganese-Induced Neurotoxicity in Rats
Melda Apaydin1,2, Oytun Erbas3, Dilek Taskiran4
1Department of Physiology, School of Medicine, Ege University, Izmir, Turkey.
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.
Insights
Excessive manganese (Mn) exposure causes neurotoxicity and motor deficits in rats. Edaravone (EDA), a radical scavenger, effectively protected against these harmful effects, suggesting its therapeutic potential.
Area of Science:
- Neuroscience
- Toxicology
- Biochemistry
Background:
- Manganese (Mn) is essential but toxic at high levels, causing manganism.
- Neurotoxicity from excessive manganese exposure is a significant health concern.
Purpose of the Study:
- To assess subacute manganese exposure effects on rat neurotoxicity.
- To evaluate edaravone's protective role against manganese-induced neurotoxicity.
- To measure manganese accumulation in the brain using MRI.
Main Methods:
- Rats were exposed to manganese, with some treated with edaravone.
- Evaluated weight gain, motor performance, and brain mitochondrial biochemical parameters (Complex I activity, lipid peroxides, protein carbonyls).
- Magnetic resonance imaging (MRI) was used to quantify manganese brain accumulation.
Main Results:
- Manganese exposure impaired motor performance, caused weight loss, and increased brain manganese levels.
- Mitochondrial oxidative stress markers (lipid peroxides, protein carbonyls) increased, while Complex I activity decreased.
- Edaravone treatment mitigated oxidative damage and improved motor function.
Conclusions:
- Subacute manganese exposure induces significant neurotoxicity and mitochondrial dysfunction in rats.
- Edaravone demonstrates protective effects against manganese-induced neurotoxicity.
- Edaravone shows potential as a therapeutic agent for manganese neurotoxicity.
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