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首页> 外文期刊>Journal of applied toxicology >Is thallium-induced nephrotoxicity in rats connected with riboflavin and/or GSH?--reconsideration of hypotheses on the mechanism of thallium toxicity.
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Is thallium-induced nephrotoxicity in rats connected with riboflavin and/or GSH?--reconsideration of hypotheses on the mechanism of thallium toxicity.

机译：th诱导的大鼠肾毒性是否与核黄素和/或GSH有关？对re毒性机理的假设的重新考虑。

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摘要

Adult female Wistar rats (Han:Wist) were injected with 2 mg of Tl2SO4 per 100 g body weight. Parameters of nephrotoxicity were urinary volume and protein excretion as well as blood urea nitrogen concentration. Thallium concentrations were determined in renal cortex and medulla. There was no effect of different schedules of vitamin B2 (riboflavin) treatment on thallium nephrotoxicity. Glutathione (GSH) concentration was not decreased by thallium in renal cortex or in medulla. The increase of GSH concentration in renal tissue by N-acetylcysteine pretreatment did not influence thallium nephrotoxicity. Buthionine sulphoximine diminished thallium nephrotoxicity by a significant decrease of thallium concentration in renal medulla, which was caused by enhanced urinary excretion of thallium. From our investigations we conclude that there is no relation between thallium-induced nephrotoxicity and riboflavin and/or GSH.
机译：成年雌性Wistar大鼠（Han：Wist）每100 g体重注射2 mg Tl2SO4。肾毒性的参数是尿量和蛋白质排泄以及血尿素氮浓度。测定肾皮质和髓质中的浓度。不同时间表的维生素B2（核黄素）治疗对th肾毒性没有影响。 renal在肾皮质或延髓中并未降低谷胱甘肽（GSH）浓度。 N-乙酰半胱氨酸预处理增加肾组织中GSH的浓度不会影响th的肾毒性。丁硫氨酸亚砜亚胺通过显着降低肾髓质中concentration的浓度而减少了ne的肾毒性，这是由于enhanced的尿排泄增加所致。根据我们的研究，我们得出结论，al诱导的肾毒性与核黄素和/或GSH之间没有关系。

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