SULPHUR-CONTAINING AMINO ACIDS METABOLISM IN EXPERIMENTAL HYPER- AND HYPOTHYROIDISM IN RATS.

Area of Science:

• Endocrinology
• Biochemistry
• Metabolic Disorders

Background:

• Thyroid hormones are crucial for metabolic regulation.
• Endocrinopathies like hyper- and hypothyroidism are common.
• The molecular mechanisms linking thyroid function to sulfur-amino acid metabolism are not fully understood.

Purpose of the Study:

• To investigate the influence of thyroid gland functional state on sulfur-containing amino acid metabolism.
• To analyze the activity of key enzymes in liver and kidneys.
• To measure blood levels of homocysteine, cysteine, and hydrogen sulfide (H2S).

Main Methods:

• Induced hyper- and hypothyroidism in rats using L-thyroxine and mercazolil.
• Confirmed thyroid states via free triiodothyronine (fT3), free thyroxine (fT4), and thyroid-stimulating hormone (TSH) levels.
• Assessed enzymatic activity in liver and kidneys and measured blood metabolite concentrations.

Main Results:

• Hypothyroidism decreased activities of remethylation and transsulfuration enzymes (S-adenosylmethionine synthase, S-adenosylhomocysteine hydrolase, betaine-homocysteine methyltransferase, cystathionine-β-synthase).
• Hypothyroidism inhibited cysteine desulfuration enzymes and increased blood homocysteine and cysteine, while decreasing H2S.
• Hyperthyroidism increased the activity of these enzymes and decreased homocysteine levels.

Conclusions:

• Thyroid dysfunction significantly alters sulfur-amino acid metabolism.
• Disruptions in remethylation, transsulfuration, and desulfuration pathways are linked to hypothyroidism.
• These metabolic changes may contribute to atherosclerosis, endothelial dysfunction, and hypercoagulation in hypothyroid states.