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丙基硫氧嘧啶或甲状腺素对大鼠肝脏中三氧化二砷毒性的影响。

Effect of n-propylthiouracil or thyroxine on arsenic trioxide toxicity in the liver of rat.

作者信息

Allen Tanu, Rana Suresh Vir Singh

机构信息

Department of Zoology, Toxicology Laboratory, Ch. Charan Singh University, Meerut, India.

出版信息

J Trace Elem Med Biol. 2007;21(3):194-203. doi: 10.1016/j.jtemb.2007.04.004. Epub 2007 Jul 5.

Abstract

Involvement of thyroid gland in the hepatotoxic manifestations of arsenic trioxide (As(III)) has been studied in rat. The effects of n-propylthiouracil (PTU) (a thyrotoxic compound) and L-thyroxine (a thyroid hormone) have been studied with reference to T(3) and T(4) values in the serum, arsenic concentration in the liver, Ca(2+) accumulation in the liver, aspartate transaminase, alanine transaminase and bilirubin values as the indicators of liver function, histopathological observations and finally the ultrastructural studies. It is concluded that hypothyroid condition protects against As(III) toxicity. Scavenging of reactive oxygen species (ROS) that significantly contribute in As(III) toxicity, by high intracellular concentration of reduced glutathione, as a consequence of PTU treatment is proposed as the plausible protective mechanism.

摘要

已在大鼠中研究了甲状腺在三氧化二砷(As(III))肝毒性表现中的作用。参照血清中的T(3)和T(4)值、肝脏中的砷浓度、肝脏中的Ca(2+)积累、作为肝功能指标的天冬氨酸转氨酶、丙氨酸转氨酶和胆红素值、组织病理学观察以及最后的超微结构研究,研究了丙基硫氧嘧啶(PTU)(一种甲状腺毒性化合物)和L-甲状腺素(一种甲状腺激素)的作用。得出的结论是,甲状腺功能减退状态可预防As(III)毒性。由于PTU治疗导致细胞内还原型谷胱甘肽浓度升高,从而清除了对As(III)毒性有显著贡献的活性氧(ROS),这被认为是可能的保护机制。

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