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丁烯内酯对分离红细胞膜的氧化损伤。

The oxidative damage of butenolide to isolated erythrocyte membranes.

作者信息

Wang Yi-Mei, Peng Shuang-Qing, Zhou Qi, Wang Min-Wei, Yan Chang-Hui, Wang Guo-Qiang, Yang Hai-Ying

机构信息

National Beijing Center for Drug Safety Evaluation and Research, Beijing Institute of Pharmacology and Toxicology, No. 27, Taiping Road, Haidian District, Beijing 100850, PR China.

出版信息

Toxicol In Vitro. 2007 Aug;21(5):863-9. doi: 10.1016/j.tiv.2007.02.009. Epub 2007 Feb 28.

Abstract

Butenolide (CAS No. 16275-44-8), a mycotoxin produced by several Fusarium species, has been shown to be a potential risk factor for animal and human health. This study was undertaken to investigate the potential oxidative damage of butenolide to biomembranes in vitro using the erythrocyte membrane model. Following exposure of isolated rat erythrocyte membranes to butenolide, the extent of oxidative damage was assessed by measuring lipid peroxidation, -SH groups content, Ca2+/Mg2+-ATPase and Na+/K+-ATPase activities, and conformational changes in membrane proteins. It was observed that butenolide resulted in a significant lipid peroxidation, revealed by a concentration-dependent increase in the level of thiobarbituric acid reactive substances (TBARS). Similarly, this toxin induced a concentration-dependent decrease in the content of membrane total -SH groups, as well as free -SH groups. Membrane-bound enzymes were also impaired by the toxin, demonstrated by the marked inhibition of the activities of Na+/K+-ATPase and Ca2+/Mg2+-ATPase. Conformational changes in membrane proteins were determined using electron paramagnetic resonance (EPR) spin labeling. Butenolide caused an increase in the ratio of weakly to strongly immobilized components (W/S ratio) in a manner of concentration-dependent, indicating conformational changes in membrane proteins occurred. In conclusion, these findings indicate that butenolide is capable of inducing significant oxidative damage to membrane lipids and proteins.

摘要

丁烯内酯(CAS编号:16275 - 44 - 8)是由几种镰刀菌属产生的一种霉菌毒素,已被证明是动物和人类健康的潜在风险因素。本研究旨在使用红细胞膜模型在体外研究丁烯内酯对生物膜的潜在氧化损伤。将分离的大鼠红细胞膜暴露于丁烯内酯后,通过测量脂质过氧化、-SH基团含量、Ca2+/Mg2+-ATP酶和Na+/K+-ATP酶活性以及膜蛋白的构象变化来评估氧化损伤程度。观察到丁烯内酯导致显著的脂质过氧化,硫代巴比妥酸反应性物质(TBARS)水平呈浓度依赖性增加表明了这一点。同样,这种毒素导致膜总-SH基团以及游离-SH基团含量呈浓度依赖性降低。膜结合酶也受到该毒素的损害,Na+/K+-ATP酶和Ca2+/Mg2+-ATP酶活性受到显著抑制证明了这一点。使用电子顺磁共振(EPR)自旋标记法测定膜蛋白的构象变化。丁烯内酯以浓度依赖性方式导致弱固定化成分与强固定化成分的比例(W/S比例)增加,表明膜蛋白发生了构象变化。总之,这些发现表明丁烯内酯能够对膜脂质和蛋白质诱导显著的氧化损伤。

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