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热皮肤损伤后α-生育酚和还原型谷胱甘肽缺乏以及红细胞变形性降低。

alpha-Tocopherol and reduced glutathione deficiency and decreased deformability of erythrocytes after thermal skin injury.

作者信息

Bekyarova G, Yankova T

机构信息

Department of Pathophysiology, Medical University, Varna, Bulgaria.

出版信息

Acta Physiol Pharmacol Bulg. 1998;23(2):55-9.

Abstract

Burns are followed by oxidative changes in red blood cells, probably as a result of ischemia/reperfusion which takes place in the microvasculature of the injured tissues. This leads to a marked decrease in the erythrocyte deformability, one of the most prominent factors for haemorheological disorders in the early post-burn period. We found that at the 24 th hour after burn skin injury of rats, the decrease in erythrocyte deformability was accompanied by an increase of fluorescent product levels in red blood cells. The erythrocyte systems for antioxidative protection fail to control the oxidative burst after burning. This was due to the decreased concentration of vitamin E (a-tocopherol) and reduced glutathione (GSH) and the increased oxidized glutathione (GSSG) in red blood cells. Both alpha-tocopherol and GSH-deficiency potentiate the susceptibility of red blood cells to oxidative membrane injury, and decrease the deformability of thermally affected erythrocytes. Treatment with alpha-tocopherol (20 ml/kg b.m., immediately after thermal skin injury) prevented the vitamin E reduction and peroxidative membrane damage of erythrocytes and improved their deformability. These results provided strong evidence that the decreased erythrocyte deformability is partly related with alpha-tocopherol deficiency and oxidative membrane damage of red blood cells in the early post burn period.

摘要

烧伤后红细胞会发生氧化变化,这可能是由于受损组织微血管中发生的缺血/再灌注所致。这会导致红细胞变形性显著降低,而红细胞变形性是烧伤后早期血液流变学紊乱的最突出因素之一。我们发现,大鼠皮肤烧伤后24小时,红细胞变形性降低的同时,红细胞中荧光产物水平升高。烧伤后红细胞的抗氧化保护系统无法控制氧化爆发。这是由于红细胞中维生素E(α-生育酚)和还原型谷胱甘肽(GSH)浓度降低,而氧化型谷胱甘肽(GSSG)增加。α-生育酚和GSH缺乏都会增强红细胞对氧化膜损伤的易感性,并降低受热影响的红细胞的变形性。热皮肤损伤后立即用α-生育酚(20ml/kg体重)治疗可防止红细胞维生素E减少和过氧化膜损伤,并改善其变形性。这些结果有力地证明,烧伤后早期红细胞变形性降低部分与α-生育酚缺乏和红细胞氧化膜损伤有关。

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