[Functioning of the oxidizing phase of the pentosephosphate pathway in rat liver in the development of vitamin B1 deficiency in the animals].

B1-hypovitaminosis was simulated in white rats of 150-170 g body mass by means of hydroxythiamin administration at a daily dose of 4, 40 or 100 mg/kg within 10 days. Concentrations of NADP and NADPH, main cofactors of 6-phosphogluconate dehydrogenase, were dissimilarly altered in the animal liver tissue depending on the antimetabolite dose administered. Kinetic characteristics of 6-phosphogluconate dehydrogenase isozymes were shifted towards more active binding of substrates in the hypovitaminosis. Total pool of metabolites, realized via 6-phosphogluconate dehydrogenase catalytic reactions and regulated by concentration of substrates, was especially sensitive to alterations in the NADP/NADPH ratio. In severe B1-hypovitaminosis caused by hydroxythiamin the rate of oxidative reactions was increased 3-10-fold.