[Changes in protein metabolism during immunization].
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Alanine Transaminase↗
Biomedical subjects
A P Lychko
Publications and source records attributed to A P Lychko.
[Changes in the biochemical indices of the functional state of the liver during antigenic action].
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Animals↗
[Influence of enzyme inducers and inhibitors of the metabolism of xenobiotics and of the coenzyme forms of vitamins B1 and B2 on the anti-inflammatory effect of voltaren].
In experiments on 245 male rats there was studied the influence of an inductor of xenobiotic metabolism enzymes, phenobarbital, an inhibitor of microsomal monooxygenases, cobalt chloride, and also coenzyme forms of vitamins B1 and B2, thiamine diphosphate and flavin mononucleotide on the anti-inflammatory effect of voltaren evaluated according to inhibition of an increase of the limb edema, a decrease of pain sensitivity, the blood level of fucose and the liver level of malondialdehyde in rats with adjuvant arthritis. Phenobarbital weakens the anti-inflammatory action of voltaren but at the same time cobalt chloride and thiamine diphosphate potentiate the therapeutic effect of voltaren. Flavin mononucleotide fails to modify the effect of voltaren but decreases however its toxicity.
Acetanilides↗
[Enzymatic activity of xenobiotic metabolism in rats with a varying body allowance of vitamin B1].
Vitamin B1 in rats induced in the liver elevation of activity of metabolic enzymes of xenobiotics bound with membranes (dimethylaniline N-demethylase, aniline n-hydroxylase, aryl esterase). At the same time activity of the cytoplasmatic enzymes alcohol dehydrogenase and glutathione-S-transferase was appreciably lowered. An additional load with thiamine (20 mg/kg) led to a drop in activity of the membrane-bound enzymes. Vitamin B1 deficiency modified the effect of the inductor phenobarbital. Additional administration of vitamin B1 to thiamine-deficient animals normalized the thiamine level in the liver, and activity of hydroxylase, aryl esterase, formaldehyde dehydrogenase, and significantly decreased demethylase activity. In vitamin B1-deficient animals high detergent concentrations significantly suppressed NADH-dichlorophenol-indophenol-reductase activity, while low concentrations activated this enzyme as compared to the control.
Animals↗
[Metabolism and toxicity of various xenobiotics in vitamin B1 deficiency and after administration of thiamine and thiamine diphosphate].
Metabolism of aminopyrine, sodium benzoate and toxicity of cyclophosphamide were studied in 185 male rats under conditions of various content of vitamin B1 in the animals. Deficiency of thiamin led to an increase in excretion of 4-aminoantipyrine and especially of its acetylated derivative. After administration of thiamin metabolism of aminopyrine was not distinctly altered, while thiamin diphosphate inhibited the drug biotransformation. In deficiency of vitamin B1 transformation of benzoic acid into hippuric acid was inhibited but formation of glucuronides was elevated. Administration of thiamin or thiamin diphosphate stimulated the benzoic acid conjugation and inhibited the glucuronides formation. Deficiency of vitamin B1 accelerated the cyclophosphamide toxicity. Preadministration of thiamin and especially of thiamin diphosphate decreased the toxic effect of cyclophosphamide.
Aminopyrine↗
[Effect of various thiamine supplies of the body on the enzyme activity in the metabolism of xenobiotics and lipid peroxidation in rat liver microsomes].
The effect of different thiamine supply of the organism on the enzymic activity in metabolism of xenobiotics and the processes of the lipid peroxidation in the liver microsomes with the application of phenobarbital, an inductor of microsomes' enzymes are studied in experiments on Wistar albino male rats. It is established that deficit of vitamin B1 increases the activity in most of processes studied in microsomes and also the intensity of lipids' peroxidation. Phenobarbital enhances the activity of microsomal oxidation irrespectively of vitamin B1 supply, whereas peroxidation of lipids is activated by phenobarbital only in animals fed on physiological doses of vitamin B1. The N-demethylation rate of dimethylaniline in experiments in vitro is inhibited by high doses of thiamine (150 microM), its derivatives inhibited this process in low concentrations (15 microM) as well.
Animals↗