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Selenoenzyme activities in selenium- and iodine-deficient sheep
Anna E Voudouri1, Stella E Chadio, John G Menegatos
1Department of Animal Nutrition, Agricultural University of Athens, 75 Iera Odos, Votanikos, Athens 11855, Greece.
Biological Trace Element Research
|September 16, 2003
Summary
Selenium and iodine deficiencies in sheep impact selenoenzyme activity and thyroid function. Combined deficiencies particularly affect hepatic Type I deiodinase activity, suggesting compensatory mechanisms for thyroid hormone regulation.
Area of Science:
- Animal Nutrition
- Biochemistry
- Endocrinology
Background:
- Selenium and iodine are essential micronutrients crucial for thyroid hormone metabolism and antioxidant defense.
- Deficiencies in these elements can disrupt physiological processes, particularly in the thyroid gland.
- Understanding the interplay between selenium and iodine is vital for animal health and productivity.
Purpose of the Study:
- To investigate the effects of single and combined selenium (Se) and iodine (I) deficiencies on selenoenzyme activities in sheep.
- To analyze the impact on thyroid hormone levels and deiodinase activities in various tissues.
- To elucidate potential compensatory mechanisms in response to nutrient deficiencies.
Main Methods:
- Twenty-four lambs were fed semisynthetic diets with controlled deficiencies: combined Se-I, Se-only, I-only, or a control diet.
- Plasma levels of thyroid hormones (T3, T4), TSH, and inorganic iodine were measured.
- Erythrocyte glutathione peroxidase (GSH-Px) activity and tissue selenoenzyme activities (ID-I, ID-II, ID-III) were analyzed.
Main Results:
- Plasma thyroid hormone and TSH levels remained similar across all groups.
- Hepatic Type I deiodinase (ID-I) activity significantly increased (70%) in combined Se-I deficiency.
- Thyroidal cystolic GSH-Px activity increased (57%) in I deficiency, while Type III deiodinase (ID-III) activity decreased in I and combined Se-I deficiencies.
Conclusions:
- Selenium and iodine deficiencies interact sensitively in sheep thyroid and brain tissues.
- Compensatory mechanisms, including increased hepatic ID-I and preserved thyroid antioxidant enzymes, likely maintain plasma T3 levels.
- These adaptations involve de novo T3 synthesis and peripheral T4 deiodination in deficient sheep.