Lipid Peroxidation, Mitochondrial Dysfunction and Neurochemical and Behavioural Deficits in Different Neurotoxic Models: Protective Role of S-allylcysteine

Experimental evidence on the protective properties of S-allylcysteine (SAC) was collected from three models exerting striatal toxicity. In the first model, SAC (120 mg kg(-1)x5) prevented lipoperoxidation (LP) and mitochondrial dysfunction (MD) in synaptosomal fractions from 1-methyl-4-phenyl-1,2,3,6-tetrahydropiridinium-treated mice (30 mg kg(-1)), but without complete restoration of dopamine levels. In the second model, SAC (300 mg kg(-1)x 3), prevented LP and MD in synaptosomes from rats infused with 6-hydroxydopamine (8 microg microl(-1)) into the substantia nigra pars compacta, but again, without total reversion of depleted dopamine levels. In the third model, SAC (100 mg kg(-1)x 1) prevented MD in synaptosomes from rats injected with 3-nitropropionic acid (10 mg kg(-1)), but in contrast to the other models, it failed to prevent LP. SAC also prevented the aberrant motor activity patterns evoked by the three toxins. Altogether, the results suggest that the antioxidant properties of SAC are responsible for partial or total preservation of neurochemical, biochemical and behavioural markers, indicating that pro-oxidant reactions underlie the neurotoxicity in these models.