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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >S-Allylcysteine, a garlic-derived antioxidant, ameliorates quinolinic acid-induced neurotoxicity and oxidative damage in rats.
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S-Allylcysteine, a garlic-derived antioxidant, ameliorates quinolinic acid-induced neurotoxicity and oxidative damage in rats.

机译：S-烯丙基半胱氨酸是大蒜来源的抗氧化剂，可改善喹啉酸诱导的大鼠神经毒性和氧化损伤。

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Excitotoxicity elicited by overactivation of N-methyl-D-aspartate receptors is a well-known characteristic of quinolinic acid-induced neurotoxicity. However, since many experimental evidences suggest that the actions of quinolinic acid also involve reactive oxygen species formation and oxidative stress as major features of its pattern of toxicity, the use of antioxidants as experimental tools against the deleterious effects evoked by this neurotoxin becomes more relevant. In this work, we investigated the effect of a garlic-derived compound and well-characterized free radical scavenger, S-allylcysteine, on quinolinic acid-induced striatal neurotoxicity and oxidative damage. For this purpose, rats were administered S-allylcysteine (150, 300 or 450 mg/kg, i.p.) 30 min before a single striatal infusion of 1 microl of quinolinic acid (240 nmol). The lower dose (150 mg/kg) of S-allylcysteine resulted effective to prevent only the quinolinate-induced lipid peroxidation (P < 0.05), whereas the systemic administration of 300 mg/kg of this compound to rats decreased effectively the quinolinic acid-induced oxidative injury measured as striatal reactive oxygen species formation (P < 0.01) and lipid peroxidation (P < 0.05). S-Allylcysteine (300 mg/kg) also prevented the striatal decrease of copper/zinc-superoxide dismutase activity (P < 0.05) produced by quinolinate. In addition, S-allylcysteine, at the same dose tested, was able to reduce the quinolinic acid-induced neurotoxicity evaluated as circling behavior (P < 0.01) and striatal morphologic alterations. In summary, S-allylcysteine ameliorates the in vivo quinolinate striatal toxicity by a mechanism related to its ability to: (a) scavenge free radicals; (b) decrease oxidative stress; and (c) preserve the striatal activity of Cu,Zn-superoxide dismutase (Cu,Zn-SOD). This antioxidant effect seems to be responsible for the preservation of the morphological and functional integrity of the striatum.
机译：N-甲基-D-天冬氨酸受体过度活化引起的兴奋性毒性是喹啉酸诱导的神经毒性的众所周知的特征。但是，由于许多实验证据表明，喹啉酸的作用还涉及活性氧的形成和氧化应激，这是其毒性模式的主要特征，因此使用抗氧化剂作为对抗这种神经毒素引起的有害作用的实验工具变得更加重要。在这项工作中，我们研究了大蒜衍生的化合物和特征明确的自由基清除剂S-烯丙基半胱氨酸对喹啉酸引起的纹状体神经毒性和氧化损伤的影响。为此目的，在大鼠纹状体单次输注1微升喹啉酸（240 nmol）之前30分钟，给其服用S-烯丙基半胱氨酸（150、300或450 mg / kg，腹膜内）。较低剂量（150 mg / kg）的S-烯丙基半胱氨酸可有效预防喹啉酸酯诱导的脂质过氧化（P <0.05），而向大鼠全身给药300 mg / kg的该化合物可有效降低喹啉酸-纹状体反应性氧的形成（P <0.01）和脂质过氧化（P <0.05）来衡量诱导的氧化损伤。 S-烯丙基半胱氨酸（300 mg / kg）还可以防止由喹啉酸盐产生的纹状体铜/锌超氧化物歧化酶活性降低（P <0.05）。此外，在相同剂量下，S-烯丙基半胱氨酸能够降低喹啉酸引起的神经毒性，该神经毒性被评价为循环行为（P <0.01）和纹状体形态改变。总而言之，S-烯丙基半胱氨酸通过与下列能力有关的机制改善了体内喹啉酸酯的纹状体毒性：（a）清除自由基; （b）降低氧化应激; （c）保留Cu，Zn-超氧化物歧化酶（Cu，Zn-SOD）的纹状体活性。这种抗氧化作用似乎负责纹状体的形态和功能完整性的保存。

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