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丙二醛是膜脂质过氧化的终产物,其积累可导致正常红细胞和镰状红细胞出现钾泄漏。

The accumulation of malonyldialdehyde, an end product of membrane lipid peroxidation, can cause potassium leak in normal and sickle red blood cells.

作者信息

Jain S K, Ross J D, Levy G J, Little R L, Duett J

机构信息

Department of Pediatrics, Louisiana State University School of Medicine, Shreveport 71130.

出版信息

Biochem Med Metab Biol. 1989 Aug;42(1):60-5. doi: 10.1016/0885-4505(89)90041-8.

Abstract

This study has examined the effect of malonyldialdehyde (MDA), an end product of lipid peroxidation, on the K+ leak in normal (AA) and sickle (SS) red blood cells (RBCs). In vitro MDA accumulation in human RBCs was accomplished by treating them with exogenous standard MDA. MDA accumulation assessed by the thiobarbituric acid reactivity of in vitro MDA-treated RBCs was comparable to the RBCs in hemolytic anemias. There was a significant K+ leak in AA RBCs after in vitro treatment with MDA. The effect of MDA on the K+ leak was greater in SS RBCs. The increase in cellular K+ leak was significantly positively correlated with the extent of MDA accumulation as assessed by thiobarbituric acid reactivity.

摘要

本研究检测了脂质过氧化终产物丙二醛(MDA)对正常(AA)和镰状(SS)红细胞(RBC)钾离子泄漏的影响。通过用外源性标准MDA处理人红细胞来实现体外MDA积累。通过体外MDA处理的红细胞的硫代巴比妥酸反应性评估的MDA积累与溶血性贫血中的红细胞相当。体外经MDA处理后,AA红细胞出现显著的钾离子泄漏。MDA对SS红细胞钾离子泄漏的影响更大。通过硫代巴比妥酸反应性评估,细胞钾离子泄漏的增加与MDA积累程度显著正相关。

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