[Effect of pyruvate, threonine, and phosphoethanolamine on acetaldehyde metabolism in rats with toxic liver injury]. / Vliianie piruvata, treonina i fosfoétanolamina na obmen éndogennogo atsetal'degida u krys s toksicheskim porazheniem pecheni.

Pyruvate dehydrogenase, threonine aldolase and phosphoethanolamine lyase can produce acetaldehyde during normal metabolism. We studied the effect of loading with the substrates of these enzymes (pyruvate, 500 mg/kg, i.p., threonine 500 mg/kg, i.p., and phosphoethanolamine, 230 mg/kg, i.p.) on the blood concentrations of endogenous acetaldehyde and ethanol and the activities of enzymes producing and oxidizing acetaldehyde in the liver of normal rats and rats with liver injury provoked by chronic carbon tetrachloride (CCl4) treatment (0.2 ml i.p. per rat, 2 times a week during 4 weeks). Blood was collected before the treatment and then 30 min and 1 h following the administration of the substrates to intact and CCl4-treated rats. Endogenous acetaldehyde and ethanol were determined by headspace GC. The CCl4 treatment resulted in decreased liver alcohol dehydrogenase and aldehyde dehydrogenase activities and a significant elevation of liver endogenous ehtanol and a clear tendency to enhance blood acetaldehyde levels. Pyruvate increased blood endogenous acetaldehyde in CCl4-treated animals and endogenous ethanol--in the control group of animals. Threonine elevated endogenous acetaldehyde in normal rats. Phosphoethanolamine increased endogenous ethanol in the intact and CCl4 groups. At the same time, in CCl4-treated rats pyruvate administration increased the liver pyruvate dehydrogenase, threonine decreased threonine aldolase, whereas phosphoethanolamine decreased phosphoethanolamine lyase. Thus, the CCl4 effect on blood endogenous acetaldehyde and ethanol may be mediated through decreased liver ALDH and ADH activities. Liver injury promotes the accumulation of acetaldehyde, derived from physiological sources, including the degration of pyruvate and threonine by decreased acetaldehyde oxidation.

[Effect of pyrazole on the activity of acetaldehyde-producing enzymes in the liver]. / Vliianie pirazola na aktivnost' atsetal'degidprodutsiruiushchikh fermentov pecheni.

Influence of pyrazole on the endogenous ethanol level and activities of acetaldehyde-producing enzymes was investigated. Drastic enhancement of the endogenous ethanol level in the blood and tissues was accompanied by an insignificant increase of phosphoethanolamine lyase activity, while activity of threonine aldolase and pyruvate dehydrogenase was unchanged.

Influence of pyruvate, threonine and phosphoethanolamine on activities of some acetaldehyde-producing enzymes.

Threonine (50 mg/100 g, i.p.) leads to increased hepatic threonine aldolase activity in rats, although endogenous ethanol concentrations remain stable. After pyruvate administration (50 mg/100 g, i.p.), endogenous blood ethanol levels are raised within 30 min, but return to normal at 60 min. The activity of threonine aldolase is decreased in the liver, whereas phosphoethanolamine lyase and pyruvate dehydrogenase activities remain unchanged. Phosphoethanolamine administration (23 mg/100 g, i.p.) did not change the endogenous ethanol concentration or pyruvate dehydrogenase, threonine aldolase and phosphoethanolamine lyase activities. Pyruvate appears to be a better precursor of acetaldehyde than threonine or phosphoethanolamine.

[Effects of nicotinamide and oxythiamine on the lipogenic parameters of the adipose tissue of mice with non-insulin-dependent type of experimental diabetes mellitus and hyperinsulinemia]. / Deistvie nikotinamida i oksitiamina na lipogennye parametry zhirovoi tkani myshei s insulinnezavisimym tipom diabeta i giperinsulinemiei.

The influence of nicotinamide and oxythiamine on the activity of NADPH-producing dehydrogenases of glucoso-6-phosphate, 6-phosphogluconate, malate, isocitrate, as well as concentration and synthesis rate of fatty acids in fatty tissue were studied in experiments on mice with genetically conditioned non-insulin-dependent diabetes and hyperinsulinemia. It has been established that in these diseases the synthesis of fatty acids and their inclusion into lipids are activated without increasing the above enzymes activity. It is shown that nicotinamide and oxythiamine inhibit inclusion of C from glucose into free fatty acids, antivitamin intensifies lipolysis in the fatty tissue of the diseased animals.

[The role of niacin in regulating the pentosophosphate pathway and production of NADP-H in fatty tissue]. / Rol' niatsina v reguliatsii pentozofosfatnogo puti i produktsii NADF-N v zhirovoi tkani.

A study was made of the effect of alimentary deficiency of niacin and of exogenous nicotinamide (500 mg/kg) on the activity of the key enzymes of the pentose phosphate pathway and NADP-dependent malate and isocitric dehydrogenase in the epididymal fatty tissue of rats. It is established that vitamin depletion in the animals' body brings about a 3-fold decrease in the content of NADP+ and a 1.7-fold decrease in the content of NADPH, a 43-percent inhibition of the activity of glucose 6-phosphate dehydrogenase and a 39-percent reduction with respect to transketolase. Nicotinamide suppresses the activity of glucose 6-phosphate dehydrogenase by 35% and that of isocitric dehydrogenase by 40% 12 hours after intraperitoneal injection. It is suggested that NADPH production in the fatty tissue of rats undergoes appreciable changes under the effect of niacin.