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首页> 外文期刊>Journal of applied toxicology >Cadmium-induced neurological disorders: prophylactic role of taurine.
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Cadmium-induced neurological disorders: prophylactic role of taurine.

机译：镉引起的神经系统疾病：牛磺酸的预防作用。

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The present study was conducted to investigate whether the conditionally essential amino acid taurine could play any protective role against the potent neurotoxin cadmium (Cd)-induced oxidative impairment in mice brain. Cd administration in the form of CdCl(2 )(at a dose of 4 mg kg(-1) body weight for 3 days, orally) increased the intracellular accumulation of metallic Cd, reactive oxygen species and super oxide radicals. The toxin also augmented the extent of lipid peroxidation, protein carbonylation and the levels of glutathione disulfide. Activities of the antioxidant enzymes and the levels of reduced glutathione as well as total thiols have been significantly decreased due to Cd exposure. In addition, the toxin also caused significant DNA degradation (as evidenced from DNA smearing and diphenylamine reaction). Oral administration of taurine (at a dose of 100 mg kg(-1) body weight for 5 days) was found to be very effective in the prevention of Cd-induced oxidative impairment in the brain tissue of experimental mice. In addition, taurine treatment could also prevent the reduction in the in vivo antioxidant power linearly up to a dose of 100 mg kg(-1) body weight. The preventive role of taurine against Cd-induced cerebral oxidative damage was supported by the observation under scanning electron microscope as well as histological examination of brain segments. To validate the experimental results, a well-known water soluble antioxidant, vitamin C, was used as the positive control in the study. In all, the results suggest that taurine plays a beneficial role against Cd-induced cerebral oxidative stress. Copyright (c) 2008 John Wiley & Sons, Ltd.
机译：进行本研究以研究条件必需氨基酸牛磺酸是否可以对小鼠脑中强力神经毒素镉（Cd）诱导的氧化损伤起任何保护作用。以CdCl（2）的形式（以4 mg kg（-1）体重的剂量连续3天进行口服Cd）可增加细胞内金属Cd，活性氧和超氧化物自由基的积累。该毒素还增加了脂质过氧化程度，蛋白质羰基化程度和谷胱甘肽二硫化物的水平。由于Cd暴露，抗氧化剂酶的活性和还原型谷胱甘肽以及总硫醇的水平已大大降低。此外，该毒素还引起了显着的DNA降解（如DNA涂片和二苯胺反应所证明）。口服牛磺酸（剂量为100 mg kg（-1）体重5天）被发现对预防Cd诱导的实验小鼠脑组织氧化损伤非常有效。此外，牛磺酸治疗还可以防止体内抗氧化能力的线性下降，直至剂量达到100 mg kg（-1）体重。牛磺酸对Cd引起的脑部氧化损伤的预防作用得到了扫描电子显微镜的观察以及脑节的组织学检查的支持。为了验证实验结果，在研究中使用了著名的水溶性抗氧化剂维生素C作为阳性对照。总之，结果表明牛磺酸在对抗Cd引起的脑氧化应激中起着有益的作用。版权所有（c）2008 John Wiley＆Sons，Ltd.

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