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Brain Res Bull. 2006 Jan 30;68(5):379-83. Epub 2005 Oct 12.

Protective effect of S-allylcysteine on 3-nitropropionic acid-induced lipid peroxidation and mitochondrial dysfunction in rat brain synaptosomes.

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1
Laboratorio de Aminoácidos Excitadores, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez S.S.A., México 14269, D.F., Mexico.

Abstract

3-Nitropropionic acid is a neurotoxin that irreversibly inhibits succinate dehydrogenase, a relevant enzyme constituting the complex II of the respiratory chain during mitochondrial electron transport. 3-Nitropropionic acid is known to produce oxidative/nitrosative stress and evokes an experimental model of Huntington's disease. In this work we evaluated the effects of the antioxidant compound and major organosulfur garlic derivative, S-allylcysteine, on lipid peroxidation and mitochondrial dysfunction induced by 3-nitropropionic acid in synaptosomal fractions from rat brain. 3-Nitropropionic acid, at concentrations ranging 0.75-2.5 mM, produced enhanced levels of lipid peroxidation, while increasing concentrations of S-allylcysteine (0.1-2 mM) decreased the peroxidative action of 3-nitropropionic acid (1 mM) in synaptosomal fractions in a concentration-dependent manner. S-Allylcysteine (0.75 mM) also prevented the 3-nitropropionic acid (1mM)-induced mitochondrial dysfunction. These findings suggest that the protective actions that S-allylcysteine exert on the in vitro neurotoxicity induced by 3-nitropropionic acid are mediated by its antioxidant properties.

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