Вісник проблем біології і медицини (Sep 2020)
THE IMPACT OF B VITAMINS ON THE FUNCTIONING OF DESULFURATION CYCLE CYSTEINE OF HYPER- AND HYPOTHYROID RATS
Abstract
This research is investigation of an influence the effect of thyroid hormones on the processes of desulfuration of cysteine in animal organs and the possibility of correcting the activity of cysteine metabolism enzymes in hyper- and hypothyroidism. The aim – to investigate in an experiment the possibility of correcting the processes of cysteine metabolism and the synthesis of hydrogen sulfide, which are violated under the influence of hyper- and hypothyroidism, using folic acid, cyanocobalamin, pyridoxine and betaine. Object and methods. The work was performed on adult male rats in which the effects of hyperthyroidism (intragastric L-thyroxine for 21 days 200 µg/kg*day), hypothyroidism (thiamazole 10 kg*day) on the reactions of desulfurization cysteine in animal organs and correction were studied disturbed under the influence of L-thyroxine and thiamazole cysteine metabolism using folic acid, cyanocobalamin, pyridoxine and betaine. In the liver and kidneys, the activity of cystathionine-β-synthase (CBS), cystathionine-γ-lyase (CSE), and cysteine aminotransferase (CAT) was determined. In the brain, the activity of CBS was determined, in the myocardium – CAT, in the blood serum – the content of hydrogen sulfide (H2 S) and the concentration of total cysteine. The experimental data were compared with the control values and data from research groups of animals with hyper- and hypothyroidism. Study results. Hyperthyroidism caused an increase in the activity in the kidneys of rats of CBS and CSE (by 21 and 100%), and in the brain only of CBS (by 60%) compared with intact animals. To a greater extent, the activity of CBS increased with the administration of vitamin B6 to animals with hyperthyroidism. The activity of CSE also increased in the liver and kidneys (by 29 and 140%) when pyridoxine was used in animals with hyperthyroidism. The activity of СAT in the kidneys and brain with the introduction of vitamin B6 with thyroxine increased by 34 and 86%. Betaine caused an increase in the activity of CBS in animals with hyperthyroidism in the brain and kidneys by 24 and 69% against the control, while the activity of CSE increased in the kidneys by 105%. The combination of B9 and B12 in the kidneys led to an increase in the activity of CBS and CSE (by 33 and 115%) compared with the group of animals without correction, and in the brain to an increase in the activity of CBS by 71%. The combination of B9 , B12, B6 and betaine in animals with hyperthyroidism led to an increase in the activity of CBS and CSE, and in the kidneys of CBS, CAT and CSE. In the brain with hyperthyroidism, the combination of B9 , B12, B6 and betaine caused an increase in the activity of CBS by 94% compared with the control. L-thyroxine did not affect the level of cysteine in the blood of experimental animals. The drugs we selected and their combination did not cause significant changes in the concentration of cysteine in the blood of rats with hyperthyroidism. Administration to animals with hyperthyroidism B6 caused an increase in the level of H2 S to a greater extent – by 27% versus control. Betaine in animals with hyperthyroidism led to an increase in H2 S level by 32%, a combination of vitamins B9 and B12 – by 31%, and a combination of all mediators by 36% compared with intact animals. Thiamazole suppressed the activity of enzymes compared to intact animals: in the kidneys, the activity of CBS, CSE and CAT, respectively, by 19, 28, 39%, in the brain, the activity of CBS by 34%. Pyridoxine led to an increase in the liver activity of CBS and CSE (by 43 and 44%) compared with the group of animals in which hypothyroidism was caused, and in the kidney, the activity of CBS, CSE, and CAT. The combination of B vitamins and betaine caused an increase in the activity of CBS and CAT (by 48 and 46%) in the liver of animals with hypothyroidism. Thiamazole caused an increase (by 40%) in the serum cysteine content of animals and a decrease in H2 S level (by 24%). Only vitamin B6 led to a decrease (by 22%) in the concentration of cysteine in the blood during hypothyroidism. B6 also caused an increase (by 23%) in the level of H2 S compared with a group of animals with hypothyroidism. B9 and B12 and a combination of all mediators caused in animals with hypothyroidism an increase in the H2 S level (by 22% and 28%) compared with the group of animals with hypothyroidism. Conclusions. Hyper- and hypothyroidism cause an imbalance in the exchange of cysteine. The preparations we have chosen and their combination do not produce a reliable effect on the level of this amino acid in hyperthyroidism, but they increase the level of hydrogen sulfide in the blood serum of animals. In hypothyroidism, vitamins B6 , B12, B9 and betaine partially prevent the disruption of cysteine metabolism and lead to an increase in the level of hydrogen sulfide in serum blood, which indicates the possibility of preventing endothelial dysfunction in hypothyroidism using these drugs.
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