Ataullakhanov F I, Zhabotinskiĭ A M, Pichugin A V, Toloknova N F
Biokhimiia. 1981 Mar;46(3):530-41.
The stationary dependence of the rate of pentose cycle in erythrocytes measured by CO2 production on the degree of glutathione reduction typical for the pentose cycle was established. The steady-state rate of oxidation from the physiological to maximal values was generated by the addition of tretbutylhydroperoxide, a substrate of the glutathione peroxidase reaction, to erythrocyte suspension at a constant rate. The steady-state rate of CO2 production was correlated with the rates of oxidant addition throughout the experiment. The parameters of the pentose cycle reactions under conditions when the maximal rate of the pentose cycle and glutathione pool (GSH+2 GSSG) are taken for 100%, coincided for all donors tested. The increase in the rate of pentose cycle from 0 to 60% of the maximal one had practically no effect on the concentration of GSH, which was as high as 90% of the overall glutathione pool, thus indicating a high stabilization degree of GSH (stabilization coefficient was about 15). A further increase of the rate up to maximal values resulted in a rapid fall of the GSH level down to 0. The data obtained support the previously described mathematical model for regulation of glutathione metabolism. The GSSG liberation from the erythrocytes was shown to be directly proportional to the stationary intracellular concentration of GSSG; the transport rate constant varied in different donors from 0.15 up to 0.6(-1). The increase of oxidation rates up to maximal values, when GSSG concentration was approximated to the glutathione pool leads to a reversible decrease of GSSG concentration, which destroys the steady-state equilibrium of the pentose cycle.
通过二氧化碳生成量测定的红细胞中戊糖循环速率对戊糖循环典型的谷胱甘肽还原程度的静态依赖性得以确立。通过以恒定速率向红细胞悬液中添加叔丁基过氧化氢（谷胱甘肽过氧化物酶反应的底物），使氧化的稳态速率从生理值达到最大值。在整个实验过程中，二氧化碳生成的稳态速率与氧化剂添加速率相关。当戊糖循环的最大速率和谷胱甘肽池（GSH + 2GSSG）取为100%时，所测试的所有供体的戊糖循环反应参数均一致。戊糖循环速率从0增加到最大值的60%，实际上对谷胱甘肽浓度没有影响，谷胱甘肽浓度高达总谷胱甘肽池的90%，这表明谷胱甘肽具有较高的稳定程度（稳定系数约为15）。速率进一步增加至最大值会导致谷胱甘肽水平迅速下降至0。所获得的数据支持了先前描述的谷胱甘肽代谢调节数学模型。红细胞中GSSG的释放显示与细胞内GSSG的静态浓度成正比；转运速率常数在不同供体中从0.15变化到0.6（-1）。当GSSG浓度接近谷胱甘肽池时，氧化速率增加至最大值会导致GSSG浓度可逆性降低，这破坏了戊糖循环的稳态平衡。
