Schuster R, Jacobasch G, Holzhütter H
Institut für Biochemie, Humboldt-Universität zu Berlin, DDR.
Biomed Biochim Acta. 1990;49(2-3):S160-5.
A mathematical model aimed at the study of erythrocyte metabolism under normal conditions and under glucose 6-phosphate dehydrogenase (G6PD) deficiency has been developed. The degree of deficiency as predicted by the model on the basis of calculated upper limits of oxidative load as well as of maximal methylene blue stimulation correlates with the individual clinical manifestation of the metabolic disease. Therefore, the model permits to judge the degree of metabolic disorder in the presence of G6PD enzymopathies if the kinetic properties of the defect enzyme are known. Experimentally accessible parameters for an assessment of the oxidative load capacity of cells in vivo are proposed. Furthermore, the model predicts that the threshold of tolerance as to energetic load is drastically reduced in the case of severe G6PD deficiency.
已经建立了一个数学模型，旨在研究正常条件下以及葡萄糖6-磷酸脱氢酶（G6PD）缺乏情况下的红细胞代谢。该模型根据计算出的氧化负荷上限以及最大亚甲蓝刺激预测的缺乏程度与代谢疾病的个体临床表现相关。因此，如果已知缺陷酶的动力学特性，该模型可以判断G6PD酶病存在时的代谢紊乱程度。提出了用于评估体内细胞氧化负荷能力的实验可及参数。此外，该模型预测，在严重G6PD缺乏的情况下，对能量负荷的耐受阈值会大幅降低。
