[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 hydroxylated pyrimidine derivatives on activities of thiamine-dependent enzymes and some parameters of lipid metabolism in mice]. / Vliianie gidroksilirovannykh proizvodnykh pirimidina na aktivnost' tiaminzavisimykh fermentov i nekotorye pokazateli obmena lipidov u myshei.

It has been found that hydroxylated pyrimidine derivatives actively participate in metabolic proceeds related to functioning of vitamin B1-dependent enzymes (transketolase, 2-oxo acid dehydrogenase). Hydroxypyrimidines also induce a significant increase in the levels of total lipids and cholesterol in the mice liver, not changing the phospholipid content.

Hepatic and pancreatic effects of polyenoylphosphatidylcholine in rats with alloxan-induced diabetes.

Polyenoylphosphatidylcholine (PPC: 100 or 300 mg kg-1 b.w., by gastric intubation for 30 days) produced a clearcut protection of the liver of rats treated with alloxan (150 mg kg-1 b.w., i.p.). The liver of rats treated with alloxan was characterized by hydropic dystrophy and lymphocytic infiltrations. Treatment with alloxan increased serum gamma-GT and ALAT activities. The liver structure of rats treated with PPC did not differ from the liver of control animals. PPC normalized the biochemical abnormalities caused by the diabetes. The number of pancreatic islets and beta/alpha cell ratio decreased in the diabetic rats. A number of beta-cells in this group did not contain granules. PPC prevented the decrease in the number of islets and the beta/alpha cell ratio in the pancreas of the diabetic rats. The intensity of staining of beta-cell granules in the pancreas of PPC-treated rats had a position intermediate between the control and diabetic groups. Alloxan increased the blood glucose content where treatment with PPC decreased this. The results suggest that PPC acts as a cytoprotector in the liver and pancreas of rats with experimental diabetes induced by alloxan.

[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.

[Lipid fractions of rat liver upon administration of ethanol and ethanolamine]. / Lipidnye fraktsii pecheni krys ri vvedenii étanola i étanolamina]

After a single intragastric administration of 25% ethanol in a dose of 1 g/kg of body mass content of total lipids, lysophosphatidyl choline, phosphatidyl ethanolamine and cardiolipin was increased while phosphatidyl choline was decreased in the rat liver tissue. At the same time, there was a decrease in the rate of 2- 14C-acetate incorporation into esters of cholesterol, total phospholipids, lysophosphatidyl choline, sphingomyelin, phosphatidyl ethanolamine and cardiolipin. Administration of ethanolamine simultaneously with ethanol contributed to normalization of the lipid spectrum, impaired by the single ethanol inoculation.

[Free amino acids in the brain in moderate alcoholization of animals and administration of ethanolamine]. / Svobodnye aminokisloty mozga pri umerennoi alkogolizatsii zhivotnykh i vvedenii étanolamina.

Content of free amino acids was studied in rat brain after moderately-acute alcohol intoxication (Ig/kg of body mass), after administration of ethanolamine (100 mg/kg), phosphoethanolamine (230 mg/kg) and/or combination of these drugs with ethanol. Ethanolamine, as distinct from phosphoethanolamine, removed the effects of alcohol. Structural similarity of ethanol and ethanolamine was apparently responsible for their antagonism.

[Free amino acids of the liver and the characteristics of the amino acid metabolism in the liver and brain after cyanamide administration to rats]. / Svobodnye aminokisloty pecheni i osobennosti obmena aminokislot pecheni i mozga pri vvedenii tsiamida krysam.

A single administration to rats of cyanamide (60 mg/kg, for 1 hour) was found to decrease the contents of cysteate, serine, glutamate, glycine, alanine, valine, methionine, isoleucine, tyrosine, ethanolamine, ornithine and histidine that may be considered as a manifestation on the drug hepatotoxicity. The activities of transaminases, glutamate dehydrogenase, pyruvate dehydrogenase remained unchanged. Cyanamide effects were considerably abolished by the supplementary ethanol administration (0.5 g/kg). Cyanamide failed to affect vitamin-dependent enzymes reflecting thiamine pyrophosphate, pyridoxal phosphate and flavine adenine dinucleotide status of the rat organism.

[Effect of oxythiamine disulfides on the pancreas and thyroid of rats]. / Vliianie disul'fidov oksitiamina na podzheludochnuiu i shchitovidnuiu zhelezy krys.

Single administration of oxythiamine (200 mg/kg) or an isomolar amount of oxythiamineamyldisulfide to rats does not change the content of insulin in 72 h, whereas oxythiaminehexyldisulfide slightly increases the blood level of the hormone. Oxythiamine and its disulfides cause changes of the thyroid indicating considerable suppression of its function. It is assumed that hormonal mediation of oxythiamine nonspecific metabolic effects results predominantly from the involvement of the thyroid hormones rather than insulin.

[Thiamine diphosphate pool and its biosynthesis in the liver in galactosamine hepatitis]. / Pul tiamindifosfata i ego biosintez v pecheni pri galaktozaminovom gepatite.

The hepatitis-like changes were induced in the liver of albino female rats weighing 120-150 g and fed on the appropriate vivarium diet by single parenteral administration of hydrochloride galactosamine in a dose of 0.9 or 1.8 mmol per 1 kg of body weight. The thiamine diphosphate level in the cytosol fraction of the liver decreased 24 h after the preparation administration, the same in blood but with the higher dose used. The activity of pyruvate dehydrogenase, a thiamine diphosphate dependent enzyme, decreased similarly. The cytosol transketolase activity lowered by 38-39%. The coenzyme biosynthesis disturbance due to a fall by 49-58% in the thiamine pyrophosphatase activity is considered to be responsible for hydrochloride galactosamine-induced decrease in the thiamine diphosphate pool. Specificity of the thiamine diphosphate pool disturbance and discoordination of thiamine diphosphate dependent enzymes in the liver are observed under administration of hydrochloride galactosamine.

[Specific activity of thiamine and oxythiamine immobilized on modified cellulose]. / Izuchenie spetsificheskoi aktivnosti immobilizovannykh na modifitsirovannoi tselliuloze tiamina i oksitiamina.

The effect of thiamine and oxythiamine preparations on the activities of vitamin B1-dependent enzymes in the body of white mice was studied. It was found that the cellulose oxythiamine derivative was similar to the initial compound in the character and intensity of its antivitamin action. It was also shown that the cellulose thiamine derivative had a prolonged effect in the body, which was manifested in a slower increase in the activities of transketolase, pyruvate dehydrogenase and in the amount of thiamine diphosphate in tissues of vitamin B1-deficient animals, as compared to the effect of thiamine.

[Characteristics of thiamine thiazolone diphosphate-induced inhibition of a pyruvate dehydrogenase complex in vitro and in intact mitochondria]. / Osobennosti ingibirovaniia tiamintiazolondifosfatom piruvatdegidrogenaznogo kompleksa in vitro i v sostave intaktnykh mitokhondrii.

Thiamine thiazolone diphosphate (TTPP) was capable of penetrating through the mitochondrial membrane and of inhibiting the pyruvate dehydrogenase complex (PDC) in intact mitochondria. TTPP depressed the activity of mammalian PDC in a mixed manner (Ki = 5.10(-8) M) and yeast pyruvate decarboxylase (Ki = 5.10(-6) M) via a competitive mechanism with respect to thiamine diphosphate. It was shown that decarboxylation of pyruvate in intact and disrupted mitochondria of rat liver and brain is less inhibited by TTPP than the overall activity of PDC determined by the formation of acetyl-CoA. It was assumed that TTPP as a transition state analog participates only in oxidative reactions (but not in simple decarboxylation of pyruvate).

[Effect of acute alcoholic intoxication on lipogenesis in the liver of rats]. / Vliianie ostroi alkogol'noi intoksikatsii na lipogenez v pecheni krys.

Thirty minutes after a single ethanol injection (4 g/kg bw, i.p.) the activity of rat liver acetyl-CoA-synthetase and ATP-citralyase was decreased. Cholesterol synthesis estimated by label incorporation from 3H2O was increased whereas the synthesis of fatty acids remained at the control level. The possibility of alternative ways of acetyl-CoA production under the conditions of acute alcoholic intoxication is discussed.