Udomratn T, Steinberg M H, Campbell G D, Oelshlegel F J
Blood. 1977 Mar;49(3):471-5.
There is little information available concerning the possible effects of ascorbic acid on glucose-6-phosphate dehydrogenase (G-6-PD) -deficient erythrocytes. We therefore studied the survival of G-6-PD-deficient cells, incubated with ascorbic acid, in rats with partial reticuloendothelial and complement blockade. Animals were pretreated with ethyl palmitate and cobra venom factor. They were then transfused with 51Cr-labeled erythrocytes which had been incubated in the presence or absence of ascorbic acid. G-6-PD-deficient cells, incubated with ascorbic acid, had impaired survival when compared to that of controls. G-6-PD-deficient cells, in the absence of ascorbic acid, had survival times equal to those of normal control erythrocytes. At the concentrations used, ascorbic acid did not appear to alter the survival of normal cells. Ascorbic acid causes premature loss of G-6-PD-deficient human erythrocytes in this rat model. On the basis of previous clinical and experimental observations, as well as this study, caution should be used when administering ascorbic acid in large doses to individuals who might be G-6-PD deficient.
关于抗坏血酸对葡萄糖-6-磷酸脱氢酶(G-6-PD)缺乏的红细胞可能产生的影响,目前几乎没有相关信息。因此,我们研究了在部分网状内皮系统和补体阻断的大鼠中,与抗坏血酸一起孵育的G-6-PD缺乏细胞的存活情况。动物先用棕榈酸乙酯和眼镜蛇毒因子进行预处理。然后给它们输注在有或没有抗坏血酸存在的情况下孵育过的51Cr标记的红细胞。与对照组相比,与抗坏血酸一起孵育的G-6-PD缺乏细胞的存活受到损害。在没有抗坏血酸的情况下,G-6-PD缺乏细胞的存活时间与正常对照红细胞的存活时间相同。在所使用的浓度下,抗坏血酸似乎不会改变正常细胞的存活。在这个大鼠模型中,抗坏血酸会导致G-6-PD缺乏的人类红细胞过早丧失。基于之前的临床和实验观察以及本研究,在给可能缺乏G-6-PD的个体大剂量施用抗坏血酸时应谨慎。