Selenium and iodine deficiency : effects on selenoprotein expression and thyroid hormone metabolism in the rat
The aims of the work described in this thesis, were to develop concurrent selenium and iodine deficiencies in rats at different stages of maturity and to study the effects on selenoprotein expression, thyroid hormone metabolism, and brain biochemistry and development. The brain and thyroid gland are able to retain selenium at the expense of the liver when dietary supplies of the micronutrient are limited. Within the brain and thyroid, available selenium is primarily directed towards the synthesis of ID-I and ID-II. The lack of change or increase in thyroidal ID-I activity, in contrast with the >90% decrease in hepatic ID-I activity, provides a compensatory mechanism to maintain plasma T3 concentrations by the decreased hepatic catabolism of T3 as well as an increased thyroidal T3 synthesis. Brain selenoenzyme activity and expression remains relatively constant in selenium deficiency. In iodine deficiency, decreased plasma T4 concentrations stimulate the increased secretion of TSH which acts on the thyroid to increase the metabolic activity of the gland. This causes an increased requirement for selenoproteins in the thyroid gland to both increase the synthesis of T4 and T3 and to protect the gland from peroxidative damage. In combined selenium and iodine deficiency, the TSH-induced increase in thyroid hormone synthesis may cause an oxidant stress on the thyroid gland through increased H2O2 production. In selenium and iodine deficiencies female rats supply available micronutrient to their offspring via milk and pups are able to activate similar compensatory mechanisms as adult rats to maintain thyroid hormone synthesis and metabolism. Brains ID-II activity is increased in iodine deficiency, regardless of selenium status, which protects against a potential decrease in brain T3 concentrations.