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维生素E缺乏大鼠空肠中的脂质过氧化与电生性离子转运

Lipid peroxidation and electrogenic ion transport in the jejunum of the vitamin E deficient rat.

作者信息

Lindley K J, Goss-Sampson M A, Muller D P, Milla P J

机构信息

Gastroenterology Unit, Institute of Child Health, London.

出版信息

Gut. 1994 Jan;35(1):34-9. doi: 10.1136/gut.35.1.34.

DOI:10.1136/gut.35.1.34
PMID:8307446
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1374628/
Abstract

Increased concentrations of reactive oxygen species in children with depleted antioxidant defences have been implicated in a cycle of malnutrition, malabsorption, and infection leading to protracted diarrhoea. A rat model of chronic vitamin E deficiency has been used to study the effects of antioxidant depletion on jejunal structure and function in vitro. Basal intestinal short circuit current (Isc), a measure of net electrogenic ion movement across the intestinal epithelium, was greater in chronically vitamin E deficient jejuna than controls, as was the electrogenic secretory response to aminophylline and Escherichia coli STa but not to bethanechol. The galactose stimulated current was also greater in vitamin E deficient jejuna. Indices of lipid peroxidation (concentrations of thiobarbituric acid reactive substances and malondialdehyde) were increased in the vitamin E deficient small bowel. Small intestinal brush border membranes from vitamin E deficient animals displayed changes in both static and dynamic components of membrane fluidity measured by steady state fluorescence polarography. The results of these studies support the hypothesis that oxidative stress in subjects with compromised antioxidant defences results in small intestinal hypersecretion, which could predispose to or perpetuate protracted diarrhoea.

摘要

抗氧化防御能力不足的儿童体内活性氧物质浓度升高,这与营养不良、吸收不良和感染的循环有关,进而导致迁延性腹泻。慢性维生素E缺乏的大鼠模型已被用于研究抗氧化剂缺乏对空肠结构和体外功能的影响。基础肠短路电流(Isc)是衡量跨肠上皮净电离子移动的指标,慢性维生素E缺乏的空肠中的基础肠短路电流比对照组更大,对氨茶碱和大肠杆菌STa的电分泌反应也是如此,但对氨甲酰甲胆碱的反应则不然。维生素E缺乏的空肠中半乳糖刺激电流也更大。维生素E缺乏的小肠中脂质过氧化指标(硫代巴比妥酸反应性物质和丙二醛的浓度)升高。通过稳态荧光极谱法测量,维生素E缺乏动物的小肠刷状缘膜在膜流动性的静态和动态成分上均显示出变化。这些研究结果支持以下假设:抗氧化防御能力受损的个体中的氧化应激会导致小肠分泌过多,这可能会引发或使迁延性腹泻持续存在。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b4d/1374628/8acf172e3c3c/gut00535-0048-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b4d/1374628/8acf172e3c3c/gut00535-0048-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b4d/1374628/8acf172e3c3c/gut00535-0048-a.jpg

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