Braun L, Puskás F, Csala M, Mészáros G, Mandl J, Bánhegyi G
Department of Medical Chemistry, Semmelweis University of Medicine, Budapest, Hungary.
Free Radic Biol Med. 1997;23(5):804-8. doi: 10.1016/s0891-5849(97)00022-1.
Ascorbate catabolism was investigated in murine and human cells unable to synthesize ascorbate due to the missing gulonolactone oxidase activity. In HepG2 cells the addition of ascorbate or dehydroascorbate resulted in high glucose production, while human erythrocytes, MCF7 cells and the cellular elements of the murine blood were able to metabolize ascorbate or dehydroascorbate to lactate. The oxidative agent menadione stimulated, while the transketolase inhibitor oxythiamine inhibited, the metabolism of dehydroascorbate in each of these three cell types. Our results suggest that ascorbate breakdown through the pentose phosphate pathway can reach the glycolytic/gluconeogenic route in different cells. In ascorbate synthesizing species the ascorbate-lactate route in peripheral cells may form a catabolic branch of an interorgan ascorbate cycle, where hepatocytes are responsible for ascorbate synthesis. The catabolic part of this cycle using exogenous ascorbate could be demonstrated even in humans cells.
在因缺乏古洛糖酸内酯氧化酶活性而无法合成抗坏血酸的小鼠和人类细胞中，对抗坏血酸分解代谢进行了研究。在HepG2细胞中，添加抗坏血酸或脱氢抗坏血酸会导致高糖生成，而人类红细胞、MCF7细胞和小鼠血液中的细胞成分能够将抗坏血酸或脱氢抗坏血酸代谢为乳酸。氧化剂甲萘醌刺激了这三种细胞类型中脱氢抗坏血酸的代谢，而转酮醇酶抑制剂氧硫胺则抑制了其代谢。我们的结果表明，通过磷酸戊糖途径的抗坏血酸分解可以在不同细胞中进入糖酵解/糖异生途径。在能够合成抗坏血酸的物种中，外周细胞中的抗坏血酸-乳酸途径可能形成器官间抗坏血酸循环的分解代谢分支，其中肝细胞负责抗坏血酸的合成。即使在人类细胞中也能证明使用外源性抗坏血酸的这个循环的分解代谢部分。
