S-Allylcysteine prevents the rat from 3-nitropropionic acid-induced hyperactivity, early markers of oxidative stress and mitochondrial dysfunction
- 作者：Marí ; a N. Herrera-Mundo ; Daniela Silva-Adaya ; Perla D. Maldonado ; Sonia Galvá ; n-Arzate ; Leticia André ; s-Martí ; nez ; Veró ; nica Pé ; rez-De La Cruz ; José ; Pedraza-Chaverrí
- 关键词：3-Nitropropionic acid ; S-Allylcysteine ; Garlic-derived compounds ; Superoxide dismutase ; Hyperactivity ; Mitochondrial reducing activity ; Antioxidant defense
- 刊名：Neuroscience Research
- 出版年：2006
- 期刊代码：53_01680102
- 类别：neu
- 出版时间：September 2006
- 卷：56
- 期：1
- 页码：39-44
- 文件大小：200 K
摘要
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-(3,5-dimethylthiazol-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.