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[关于抗坏血酸诱导人红细胞高铁血红蛋白还原的机制(作者译)]

[On the mechanism of ascorbic acid induced methemoglobin reduction of human erythrocytes (author's transl)].

作者信息

Waller H D, Benöhr H C, Tigges F J

出版信息

Klin Wochenschr. 1977 Oct 1;55(19):955-64. doi: 10.1007/BF01479227.

Abstract

Ascorbic acid and dehydroascorbic acid penetrate the human erythrocyte membrane. In vitro methemoglobin is reduced nonenzymatically by both substances in concentrations of 10(-2) M to 10(-3) M. Dehydroascorbic acid is reduced nonenzymatically to ascorbic acid by GSH, even with low GSH-content of erythrocytes. Under physiological conditions ascorbic acid induced methemoglobin reduction is far less important than reduction by the NADH dependent methemoglobin reductase system. In methemoglobinemic conditions caused by toxic effects or by congenital methemoglobin reductase deficiency treatment with ascorbic acid is possible. However, critically increased methemoglobin content of the blood higher than 30% makes therapy with methylene blue necessary.

摘要

抗坏血酸和脱氢抗坏血酸可穿透人红细胞膜。在体外,浓度为10⁻²M至10⁻³M的这两种物质均可非酶促地还原高铁血红蛋白。即使红细胞中谷胱甘肽(GSH)含量较低,脱氢抗坏血酸也可被GSH非酶促地还原为抗坏血酸。在生理条件下,抗坏血酸诱导的高铁血红蛋白还原远不如依赖烟酰胺腺嘌呤二核苷酸(NADH)的高铁血红蛋白还原酶系统的还原作用重要。在由毒性作用或先天性高铁血红蛋白还原酶缺乏引起的高铁血红蛋白血症情况下,可用抗坏血酸进行治疗。然而,当血液中高铁血红蛋白含量严重增加超过30%时,则需要用亚甲蓝进行治疗。

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