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Monoamine Oxidase Inhibitors Attenuate Cytotoxicity of 1-Methyl-4-phenylpyridinium by Suppressing Mitochondrial Permeability Transition  

Lee, Chung-Soo (Department of Pharmacology, College of Medicine, Chung-Ang University)
Publication Information
The Korean Journal of Physiology and Pharmacology / v.10, no.4, 2006 , pp. 207-212 More about this Journal
Abstract
Mitochondrial permeability transition has been shown to be involved in neuronal cell death. Mitochondrial monoamine oxidase (MAO)-B is considered to play a part in the progress of nigrostriatal cell death. The present study examined the effect of MAO inhibitors against the toxicity of 1-methyl-4-phenylpyridinium $(MPP^+)$ in relation to the mitochondrial permeability transition. Chlorgyline (a selective inhibitor of MAO-A), deprenyl (a selective inhibitor of MAO-B) and tranylcypromine (nonselective inhibitor of MAO) all prevented cell viability loss, cytochrome c release, caspase-3 activation, formation of reactive oxygen species and depletion of GSH in differentiated PC12 cells treated with $500\;{\mu}M$$MPP^+$. The MAO inhibitors at $10\;{\mu}M$ revealed a maximal inhibitory effect and beyond this concentration the inhibitory effect declined. On the basis of concentration, the inhibitory potency was tranylcypromine, deprenyl and chlorgyline order. The results suggest that chlorgyline, deprenyl and tranylcypromine attenuate the toxicity of $MPP^+$ against PC12 cells by suppressing the mitochondrial permeability transition that seems to be mediated by oxidative stress.
Keywords
Monoamine oxidase inhibitors; $MPP^+$; Mitochondrial permeability transition; Cell death; Preventive effect;
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