Hino Y, Minakami S
J Biol Chem. 1983 Feb 10;258(3):1415-8.
An oxidative metabolism of glucose 6-phosphate was studied in rat liver microsomal fraction. Although radioactive 14CO2 was formed from [1-14C]glucose 6-phosphate in the microsomal fraction (Hino, Y., and Minakami, S. (1982) J. Biochem. (Tokyo) 92, 547-557), the formation was negligible when [2-14C]glucose 6-phosphate was used as a starting substrate. These results indicated an inability of the microsomal fraction to rearrange [2-14C]glucose 6-phosphate to form [1-14C] glucose 6-phosphate, and it was expected that a certain compound derived from glucose 6-phosphate accumulated as an end-product of the reaction. We, therefore, have tried to identify the product by high performance liquid chromatography, and found that ribose accumulated as the end-product. The formation of ribose was inhibited in the same manner as that of 14CO2 by antibodies against rat liver microsomal hexose-6-phosphate dehydrogenase, and the ratios of ribose to 14CO2 formed in the reaction were 0.5-0.8 on a molar basis. The finding of ribose formation further suggested the involvement of ribose phosphate isomerase and phosphatase activities in the reaction.
在大鼠肝脏微粒体部分研究了6-磷酸葡萄糖的氧化代谢。尽管在微粒体部分[1-14C]6-磷酸葡萄糖生成了放射性14CO2（日野洋，水波史郎（1982年）《生物化学杂志》（东京）92卷，547 - 557页），但当使用[2-14C]6-磷酸葡萄糖作为起始底物时，生成量可忽略不计。这些结果表明微粒体部分无法将[2-14C]6-磷酸葡萄糖重排形成[1-14C]6-磷酸葡萄糖，并且预计某种源自6-磷酸葡萄糖的化合物作为反应的终产物会积累。因此，我们试图通过高效液相色谱法鉴定该产物，发现核糖作为终产物积累。抗大鼠肝脏微粒体己糖-6-磷酸脱氢酶的抗体以与抑制14CO2生成相同的方式抑制核糖的生成，并且反应中生成的核糖与14CO2的摩尔比为0.5 - 0.8。核糖生成的这一发现进一步表明磷酸核糖异构酶和磷酸酶活性参与了该反应。
