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镉诱导的神经紊乱:牛磺酸的预防作用

Cadmium-induced neurological disorders: prophylactic role of taurine.

作者信息

Sinha Mahua, Manna Prasenjit, Sil Parames C

机构信息

Department of Chemistry, Bose Institute, Kolkata, India.

出版信息

J Appl Toxicol. 2008 Nov;28(8):974-86. doi: 10.1002/jat.1363.

DOI:10.1002/jat.1363
PMID:18548748
Abstract

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.

摘要

本研究旨在探讨条件必需氨基酸牛磺酸是否能对强效神经毒素镉(Cd)诱导的小鼠脑氧化损伤发挥保护作用。以CdCl₂的形式给予镉(剂量为4 mg/kg体重,口服,持续3天)会增加金属镉、活性氧和超氧自由基的细胞内积累。该毒素还会增加脂质过氧化程度、蛋白质羰基化程度以及谷胱甘肽二硫化物水平。由于镉暴露,抗氧化酶的活性、还原型谷胱甘肽水平以及总硫醇水平均显著降低。此外,该毒素还导致了显著的DNA降解(从DNA涂片和二苯胺反应可证明)。发现口服牛磺酸(剂量为100 mg/kg体重,持续5天)对预防实验小鼠脑组织中镉诱导的氧化损伤非常有效。此外,牛磺酸处理还可以线性地预防体内抗氧化能力的降低,直至剂量达到100 mg/kg体重。扫描电子显微镜观察以及脑切片的组织学检查结果支持了牛磺酸对镉诱导的脑氧化损伤的预防作用。为验证实验结果,在研究中使用了一种著名的水溶性抗氧化剂维生素C作为阳性对照。总之,结果表明牛磺酸对镉诱导的脑氧化应激具有有益作用。

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