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

G Bekyarova, T Yankova
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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.

-生育酚和谷胱甘肽缺乏症,以及皮肤热损伤后红细胞变形能力降低。
烧伤后红细胞发生氧化变化,这可能是损伤组织微血管发生缺血/再灌注的结果。这导致红细胞变形能力显著降低,这是烧伤后早期血液流变学障碍的最重要因素之一。我们发现,大鼠皮肤烧伤后24小时,红细胞变形能力下降,同时红细胞荧光产物水平升高。红细胞系统的抗氧化保护不能控制燃烧后的氧化爆发。这是由于红细胞中维生素E (a-生育酚)和谷胱甘肽(GSH)的浓度降低以及氧化谷胱甘肽(GSSG)的增加。α -生育酚和gsh缺乏症均可增强红细胞对氧化膜损伤的敏感性,降低热影响红细胞的变形能力。在热皮肤损伤后立即给予α -生育酚(20 ml/kg b.m),可防止红细胞维生素E减少和过氧化膜损伤,并改善其变形能力。这些结果有力地证明,红细胞变形能力下降与烧伤后早期红细胞α -生育酚缺乏和氧化膜损伤有关。
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