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[Effect of vitamin K on lipid peroxidation in E-avitaminosis].

Content of malonic dialdehyde was increased 2-fold in liver homogenates of E-avitaminous animals and 5-fold in muscle homogenates. In animals, maintained at E-avitaminous diet but treated with vitamin K, content of malonic dialdehyde in liver homogenates was similar to its content in controls; it increased only 2-fold in muscle homogenates.

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[Possibility of preventing muscular dystrophy in E avitaminosis with alpha-tocopheronolactone and diludin].

The efficacy of pharmacopeial alpha-tocopheryl acetate, alpha-tocopheronolactone and the antioxidant diludin was studied as to the possibilities of preventing E-hypovitaminosis muscle dystrophy in rabbits. alpha-Tocopheronolactone action was similar to that of pharmacopeial alpha-tocopheryl acetate as regards E-vitamin activity that was manifested by an increase in the body mass, decrease in the urine creatine index and maintenance of normal ubiquinone content, as well as of succinate-ubiquinone-reductase, NADH-ubiquinone-reductase and NADH-cytochrome c-reductase activity of rabbit skeletal muscle and heart mitochondria. On the contrary , as a result of the antioxidant administration, no direct correlation was found between ubiquinone content and activity of ubiquinone-dependent enzymatic systems of mitochondria. The data obtained attest to high E-vitamin activity of alpha-tocopheronolactone. The action of the latter was disclosed to be different from that produced by the antioxidant.

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[Effect of flavin coenzymes on the pyridoxine treatment of avitaminosis B6].

Studies on rats with experimental vitamin B6 deficiency have shown that the combined use of pyridoxine and flavine coenzymes affects the supply of rats with these vitamins. Flavine coenzymes have been found to promote more efficient normalization of pyridoxine and riboflavin balance in the body and to improve the general status of the animals, to increase the excretion of riboflavin and 4-pyridoxic acid with urine, to prove more rapid cure of vitamin deficiency.

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PubMedDate not supplied

[Pyruvate metabolism in rats with dietary B1 avitaminosis].

The influence of alimentary deficiency of thiamine on the pyruvate metabolism in the liver and blood of rats was investigated. Note is taken of a fallen activity of pyruvate-dehydrogenase (PDH) and a rising level of pyruvate in the blood and liver. An inverse relationship between the PDH activity and the pyruvate content in the liver, observed during the whole course of the experiment is in evidence, although the substrate level exceeds significantly that of the control only starting from the 20th day. In the normalization of the pyruvate level in the liver all the studied enzymatic systems partake; they join stagewise in the order of alanine-aminotransferase, pyruvate-kinase, malate-enzyme, which differently change their activity in the course of the experiment, along with physiological mechanisms of the pyruvate transport into the blood. These are most pronounced starting from the 20th day (inverse relationships of the pyruvate levels in the blood and liver). During the whole of the experiment a direct relation between the lactate content in the blood and liver persists. In these tissues no relation between the pyruvate and lactate levels was revealed.

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[On vitamin B1 metabolism in avitaminosis and its correction with thiamine and taurine].

The levels of phosphate esters and the activities of thiamine biotransformation enzymes in the blood and tissues of albino rats were studied during oxythiamine-induced B1 deficiency and after metabolic correction with thiamine and taurine. Among thiamine phosphates, the most informative indicators of thiamine deficiency were shown to be triphosphate esters and free thiamine diphosphate. The biosynthetic enzymes thiamine kinase and thiamine diphosphate kinase played a decisive role in maintaining the initial rate and in recovering the physiologically active forms of vitamin B1. The activation of hydrolytic enzymes of thiamine phosphate esters occurred by producing abundant free thiamine diphosphate and thiamine triphosphate. Within the first hours, taurine favoured the acceleration of phosphoester biosynthesis and, accumulating in the tissues, inhibited vitamin phosphorylation reactions.

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PubMedDate not supplied

[Blood transketolase activity and the TDP effect as indices of thiamine body allowance].

Protein-bound and free forms of thiamin diphosphate (TDP) (separated by dialysis and gel filtration) were found in rat erythrocytes. Content of TDP in blood did not correlate with the transketolase activity at the initial steps of B1 avitaminosis. Decrease of the DTP total amount in blood by more than 80% did not affect distinctly the transketolase activity. As shown by binding of 14C-TDP during the equilibrium dialysis and gel filtration, the apotransketolase did not occur in erythrocytes of thiamin-deficient rats. Activation of transketolase, which occurred after addition of 50 mg TDP into the whole blood lysates (TDP-effect), was characteristic for the later steps of the avitaminosis; it depended rather on leukocyte than on erythrocyte transketolase. Estimation of TDP concentration in blood was the most suitable assay for a body providing with thiamin at the early steps of the avitaminosis. The accuracy of the coenzyme estimation was decreased within 15-30 days of the avitaminosis due to its drastic lowering. In this case, determination of the transketolase activity was the most suitable criterion. The thiamin-binding protein, found in erythrocytes, appears to participate in transport of the vitamin across erythrocyte membranes.

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