期刊
NEUROSCIENCE RESEARCH
卷 56, 期 1, 页码 39-44出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.neures.2006.04.018
关键词
3-nitropropionic acid; S-allylcysteine; garlic-derived compounds; superoxide dismutase; hyperactivity; mitochondrial reducing activity; antioxidant defense
We investigated the effects of S-allylcysteine (SAC) on early behavioral alterations, striatal. changes in superoxide dismutase (SOD) activity, lipid peroxidation (LP) and mitochondrial dysfunction induced by the systemic infusion of 3-nitropropionic acid (3-NPA) to rats. SAC (300 mg/kg, i.p.), given to animals 30 min before 3-NPA (30 mg/kg, i.p.), prevented the hyperkinetic pattern evoked by the toxin. In addition, 3-NPA alone produced decreased activities of manganese- (Mn-SOD) and copper/zinc-dependent superoxide dismutase (Cu,Zn-SOD), increased LP (evaluated as the formation of lipid fluorescent products) and produced mitochondrial dysfunction in the striatum (measured as decreased 3-(3,5dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide reduction). In contrast, pretreatment of 3-NPA-injected rats with SAC resulted in a significant prevention of all these markers. Our findings suggest that the protective actions of SAC are related with its antioxidant properties, which in turn may be accounting for the preservation of SOD activity and primary mitochondrial tasks. (c) 2006 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.
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