Gorbach Z V, Maglysh S S, Nefedov L I, Ostrovskiĭ Iu M
Biokhimiia. 1987 Jan;52(1):42-52.
Vitamin B1 deficiency in mongrel albino rats induced by oxythiamine is concomitant with an increase in the ratio of free forms of NAD+/NADH, NADP+/NADPH in liver mitochondria. This is accompanied with a rise in steady-state concentrations of isocitrate, 2-oxoglutarate and with a decrease of malate in liver tissue, which testifies to the prominent regulatory role of the 2-oxoglutarate dehydrogenase complex in the intracellular metabolism under vitamin B1 deficiency. Moderate physical load causes a 10-fold increase in the steady-state concentration of pyruvate and lactate in the blood of thiamine-deficient animals, which seems to be due to the stimulation of glycolysis in the maintenance of energy homeostasis. The observed increase in the excretion of pyruvate, lactate, 2-oxoglutarate (30-fold against control) and pentose phosphates (3-fold) with urine, depending on the degree of vitamin B1 deficiency, points to one of essential mechanisms of cell metabolism stabilization under the given pathological condition.
由氧硫胺素诱导的杂种白化大鼠维生素B1缺乏症,伴随着肝脏线粒体中NAD⁺/NADH、NADP⁺/NADPH游离形式比例的增加。这伴随着肝脏组织中异柠檬酸、2-氧代戊二酸稳态浓度的升高以及苹果酸浓度的降低,这证明了2-氧代戊二酸脱氢酶复合物在维生素B1缺乏时细胞内代谢中的重要调节作用。适度的体力负荷会使硫胺素缺乏动物血液中丙酮酸和乳酸的稳态浓度增加10倍,这似乎是由于糖酵解受到刺激以维持能量稳态。观察到的丙酮酸盐、乳酸盐、2-氧代戊二酸盐(比对照组高30倍)和戊糖磷酸随尿液排泄量的增加,取决于维生素B1缺乏的程度,这指出了在给定病理条件下细胞代谢稳定的重要机制之一。