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T-2毒素暴露途径对小鼠肝脏氧化损伤的差异影响。

Differential effects of route of T-2 toxin exposure on hepatic oxidative damage in mice.

作者信息

Chaudhary Manjari, Bhaskar A S B, Rao P V Lakshmana

机构信息

Division of Pharmacology and Toxicology, Defence Research and Development Establishment, Jhansi Road, Gwalior, Madhya Pradesh, 474002, India.

出版信息

Environ Toxicol. 2015 Jan;30(1):64-73. doi: 10.1002/tox.21895. Epub 2013 Aug 9.

Abstract

T-2 toxin is the most toxic among mycotoxins and poses a potential health hazard for both humans and animals. At high doses, T-2 toxin can cause shock-like syndrome that can result in death. We evaluated the effect of time course and route of exposure on hepatic oxidative damage in mice and it is only such study so far to compare the effects of dermal and subcutaneous exposure of T-2 toxin. Mice were exposed to 1 LD50 of T-2 toxin either by percutaneous (5.94 mg/kg body weight) or subcutaneous (1.54 mg/kg body weight) route and sacrificed at 0, 1, 3, and 7 days postexposure. Analysis of a number of serum biochemical variables, antioxidant enzymes activity, gene and protein expression by immunoblot assay showed time and route dependent effects of T-2 induced hepatic oxidative damage. Time dependent increase in protein carbonyl content and protein oxidation was seen in serum and liver. Results of our study may provide possible mechanism for developing medical countermeasures against T-2 toxin.

摘要

T-2毒素是霉菌毒素中毒性最强的,对人类和动物都构成潜在的健康危害。高剂量时,T-2毒素可引发类似休克的综合征,甚至导致死亡。我们评估了接触时间过程和途径对小鼠肝脏氧化损伤的影响,这是迄今为止唯一一项比较T-2毒素经皮和皮下接触影响的研究。小鼠通过经皮(5.94毫克/千克体重)或皮下(1.54毫克/千克体重)途径接触1个半数致死剂量的T-2毒素,并在接触后0、1、3和7天处死。通过免疫印迹分析若干血清生化变量、抗氧化酶活性、基因和蛋白质表达,结果显示T-2诱导的肝脏氧化损伤具有时间和途径依赖性效应。在血清和肝脏中观察到蛋白质羰基含量和蛋白质氧化随时间增加。我们的研究结果可能为开发针对T-2毒素的医学对策提供可能的机制。

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