The research deals with the study of lipid and protein peroxidation, antioxidant defense, metabolism of nitric oxide, blood lipid spectrum and protein metabolism in rats with combined deficiencies of iodine and iron and determines the effectiveness of correction of detected changes by microelements, antioxidants and nitric oxide donators. The research was carried out on rats weighting 120-150 g that were divided into five research groups: Group I included animals with iodine deficiency (the comparison group, n=30); Group II comprised animals with combined iodine and iron deficiencies (n=30); Group III included animals with correction of combined iodine and iron deficiencies using iodine-containing drugs (potassium iodide, n=30); Group IV comprised animals with correction of combined iodine and iron deficiencies using iodine-containing drugs and iron hydroxide (n=30); Group V consisted of animals with correction of combined iodine and iron deficiencies using iodine, iron, antioxidants, nitric oxide donators (n=30). In order to induce iodine deficiency all animals were kept on iodine-deficient diet for 45 days and received merkazolil with drinking water (7.5 mg/100 g body weight). Iron deficiency was induced by daily intraperitoneal injection of chelator deferoxamine at a dose of 20 mg/100 g body weight since 31st to 45th days of the experiment. The correction was carried out by addition of potassium iodide (50 mg daily for 30 days), iron hydroxide (2.5 mg daily for 20 days), alpha-tocopherol acetate (20 mg daily for 30 days), L-arginine hydrochloride (2.5 g daily for 20 days) to diet. The control group consisted of 30 animals, which received intraperitoneal injection of physiologic solution (0.2 ml/100 g body weight) since 31st to 45th days of the experiment. Iodine deficiency and combined microelement deficiency were found to be accompanied by impaired thyroid profile as indicated by a decrease in serum levels of free triiodothyronine (fT3) and thyroxine (fT4) on the background of increased TSH. In animals with iodine deficiency the activation of lipid peroxidation, the suppression of most studied antioxidant enzymes (excluding the catalase and glutathione peroxidase the levels of which increased) and the development of dyslipidemia were observed. Iron deficiency negatively affected prooxidant-antioxidant homeostasis in rats, potentiated changes in blood lipid spectrum that could significantly increase the risk for the development of disturbances associated with goiter. The correction of revealed changes was effective when using potassium iodide. The effectiveness and rationale of adding iron hydroxide, antioxidants (alpha-tocopherol acetate) and nitric oxide donators (L-arginine hydrochloride) to the therapeutic scheme for correcting metabolic disturbances and preventing comorbid pathology in hypothyroid dysfunction were determined
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