Domke I, Weis W
Int J Vitam Nutr Res. 1983;53(1):51-60.
To investigate the diabetogenic effect of pure dehydroascorbic acid, male Wister- and Sprague-Dawley rats received i.v. injections of the substance. No hyperglycemia and no decreased glucose tolerance were found. I.v. administration of the hydrolysis products of dehydroascorbic acid and of a solution containing monodehydroascorbate likewise did not increase blood glucose values. It is concluded that in previously performed experiments not dehydroascorbic acid itself but one or several impurities might have produced hyperglycemia in the rat. The electron transfer proteins tested (ascorbate:ferricytochrome b5 oxidoreductase, cytochrome b5, NADH:ferricytochrome b5 oxidoreductase, NADH:monodehydroascorbate oxidoreductase), which might participate in the reduction of dehydroascorbic acid, could not be induced in liver microsomes from Wistar rats by the injection of dehydroascorbic acid, its hydrolysis products, or monodehydroascorbate.
为研究纯脱氢抗坏血酸的致糖尿病作用，对雄性Wistar大鼠和Sprague-Dawley大鼠进行了该物质的静脉注射。未发现高血糖和葡萄糖耐量降低。静脉注射脱氢抗坏血酸的水解产物和含有单脱氢抗坏血酸的溶液同样未使血糖值升高。得出的结论是，在先前进行的实验中，可能不是脱氢抗坏血酸本身，而是一种或几种杂质导致大鼠出现高血糖。所测试的电子传递蛋白（抗坏血酸：铁细胞色素b5氧化还原酶、细胞色素b5、NADH：铁细胞色素b5氧化还原酶、NADH：单脱氢抗坏血酸氧化还原酶）可能参与脱氢抗坏血酸的还原，但通过注射脱氢抗坏血酸、其水解产物或单脱氢抗坏血酸，无法在Wistar大鼠的肝微粒体中诱导这些蛋白产生。
