CORRECTION BY VITAMINS OF GROUP B IN DISTURBANCES OF HOMOCYSTEIN UTILIZATION IN TRANSCULTURATION PATHWAY IN HYPER- AND HYPOFUNCTIONS OF THE THYROID

Abstract

Introduction. Thyroid dysfunction is a factor in the development of many cardiovascular diseases, at the same time, hyperhomocysteinemia is also a well-known factor in the development of pathologies of the cardiovascular system. It was found that experimental hyperthyroidism causes a decrease in the level of homocysteine ​​(HCy) in the blood, while hypothyroidism leads to opposite changes in the exchange of sulfur-containing amino acids, in particular, an increase in the HCy content in the blood, a decrease in the level of H₂S and an increase in the level of cysteine, which is a consequence of changes in the activity of enzymes metabolism of methionine.

The aim of the study – to elucidate the effect of thyroid hormones on the processes of HCy transsulfuration in animal organs and to assess the possibility of correcting HCy metabolism disturbed under the influence of hyper- and hypothyroidism with the help of vitamins B₆, B₉, B₁₂ and betaine.

Research Methods. The work was performed on male rats, in which the effect of hyper- (L-thyroxine, 200 μg/day per 1 kg of body weight) and hypothyroidism (thiamazole, 10 mg/day per 1 kg of body weight) on the reaction of transsulfuration HCy in animal organs and disturbed under the influence of L-thyroxine and thiamazole the metabolic processes of HCy with the help of vitamins B₆, B₉, B₁₂ and betaine. In the liver and kidneys, the cystathionine synthase activity of cystathionine-β-synthase (CBS) and the cystathionine-γ-lyase (CSE) activity were determined, in the brain – only the activity of CBS, in the blood – the content of HCy and cysteine.

Results and Discussion. Hyperthyroidism caused an increase in the cystathionine synthase activity of CBS in the liver and brain. The use of vitamin B₆ in animals with hyperthyroidism led to an even greater increase in this indicator. The cystathioninase activity of CSE in hyperthyroidism and the use of B₆ significantly increased only in the kidneys. Betaine, B₉ and B₁₂ in animals with hyperthyroidism caused an increase in the activity of CSE in the brain and liver. Hyperthyroidism lowers HC levels and does not affect cysteine ​​levels. Folic acid, cyanocobalamin, pyridoxine, and betaine, when administered in parallel with L-thyroxine, partially prevented a decrease in the concentration of HC in the blood. Thiamazole suppressed the activity of enzymes of the transsulfuration pathway in comparison with intact animals: CSE – in the liver and kidneys, CSE – in the kidneys. Pyridoxine partially prevented a decrease in the activity of CBL in the liver and brain, betaine – the activity of CSE in the tissues of the liver, kidneys and brain, and only in the kidneys of the activity of CSE. The combination of B vitamins and betaine proved to be effective. Hypothyroidism led to increased blood levels of HCy and cysteine. Vitamin B₆, B₉ and B₁₂, as well as the combination of all mediators, caused a decrease in the level of HCy in animals with hypothyroidism.

Conclusions. Our results indicate that long-term hyper- and hypothyroidism cause an imbalance in the HCy transsulfuration pathway. Folic acid, cyanocobalamin, pyridoxine and betaine partially prevent the disturbance of the metabolic processes of sulfur-containing amino acids and lead to a decrease in the level of HCy and cysteine ​​in the blood of rats with hypothyroidism.