Herrera-Mundo María N, Silva-Adaya Daniela, Maldonado Perla D, Galván-Arzate Sonia, Andrés-Martínez Leticia, Pérez-De La Cruz Verónica, Pedraza-Chaverrí José, Santamaría Abel
Laboratorio de Aminoácidos Excitadores, Instituto Nacional de Neurología y Neurocirugía, México DF, Mexico.
Neurosci Res. 2006 Sep;56(1):39-44. doi: 10.1016/j.neures.2006.04.018. Epub 2006 Jun 27.
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.
我们研究了S-烯丙基半胱氨酸（SAC）对全身注射3-硝基丙酸（3-NPA）诱导的大鼠早期行为改变、纹状体超氧化物歧化酶（SOD）活性变化、脂质过氧化（LP）及线粒体功能障碍的影响。在腹腔注射3-NPA（30mg/kg）前30分钟给动物腹腔注射SAC（300mg/kg），可预防毒素诱发的运动亢进模式。此外，单独注射3-NPA会导致锰超氧化物歧化酶（Mn-SOD）和铜/锌依赖性超氧化物歧化酶（Cu,Zn-SOD）活性降低，脂质过氧化增加（以脂质荧光产物的形成来评估），并在纹状体中产生线粒体功能障碍（以3-(3,5-二甲基噻唑-2-基)-2,5-二苯基四氮唑溴盐还原能力降低来衡量）。相比之下，用SAC预处理注射3-NPA的大鼠可显著预防所有这些指标的变化。我们的研究结果表明，SAC的保护作用与其抗氧化特性有关，这反过来可能是其维持SOD活性和线粒体主要功能的原因。
