Up to one billion people live in areas where they may be at risk from I deficiency. Many of the debilitating effects of the deficiency may be irreversible, consequently it is essential to understand the mechanisms whereby lack of I can cause disease through decreased thyroxine and 3, 3',5-triiodothyronine (T3) synthesis. Since Se has an essential role in thyroid hormone metabolism, it has the potential to play a major part in the outcome of I deficiency. These effects of Se derive from two aspects of its biological function. First, three Se-containing deiodinases regulate the synthesis and degradation of the biologically active thyroid hormone, T3. Second, selenoperoxidases and possibly thioredoxin reductase (EC 1.6.4.5) protect the thyroid gland from H2O2 produced during the synthesis of thyroid hormones. The mechanisms whereby Se deficiency exacerbates the hypothyroidism due to I deficiency have been elucidated in animals. In contrast to these adverse effects, concurrent Se deficiency may also cause changes in deiodinase activities which can protect the brain from low T3 concentrations in I deficiency. Animals with Se and I deficiency have changes in serum thyroid hormone concentrations that are similar to those observed in patients with I deficiency disease. However such animal models show no thyroid involution, a feature which is characteristic of myxoedematous cretinism in man. These observations imply that if Se deficiency is involved in the outcome of I deficiency in human populations it is likely that other interacting factors such as goitrogens are also implicated. Nevertheless the protection of the thyroid gland from H2O2 and the regulation of tissue T3 levels are the functions of Se that are most likely to underlie the interactions of Se and I.

Excessive iodine induces thyroid dysfunction. However, the effect of excessive iodine exposure on maternal–fetal thyroid hormone metabolism and on the expression of genes involved in differentiation, growth and development is poorly understood. Since a thyroid hormone receptor response element was found in the Hoxc8 promoter region, Hoxc8 expression possibly regulated by excessive iodine exposure was firstly investigated. In the present study, Balb/C mice were given different doses of iodine in the form of potassium iodate (KIO3) at the levels of 0 (sterile water), 1·5, 3·0, 6·0, 12·0 and 24·0 μg/ml in drinking water for 4 months, then were mated. On 12·5 d postcoitum, placental type 2 and type 3 deiodinase activities and fetal Hoxc8 expression were determined. The results showed that excessive iodine exposure above 1·5 μg/ml resulted in an increase of total thyroxine and a decrease of total triiodothyronine in the serum of maternal mice, which was mainly associated with the inhibition of type 1 deiodinase activity in liver and kidney. Placental type 2 deiodinase activity decreased, showing an inverse relationship with maternal thyroxine level. Hoxc8 mRNA and protein expression at 12·5 d postcoitum embryos were down regulated. Because Hoxc8 plays an important role in normal skeletal development, this finding provides a possible explanation for the skeletal malformation induced by excessive iodine exposure and also provides a new clue to study the relationship between iodine or thyroid hormones and Hox gene expression pattern.

The effects of nutrition on patterns of live-weight change, hair follicle activity, moult, hormone profiles and associated activities of monodeiodinase enzyme types II and III (MDII and MDIII) in cashmere goats were investigated. From 1 week before the winter solstice (mid December), one group of 15 animals was given a ration designed to provide 2·0 × live weight maintenance requirements (high; H) while a second, similar, group was given 0·8 × live weight maintenance requirements (low; L). After approximately 3 months, L animals had significantly lower mean live weights (P<0·01) than H animals. This was associated with lower (P<0·05) overall mean hair follicle activity in L than H animals during the March to May period and a lower overall mean moult score during March and April in L animals (P<0·01) but a similar mean date of moult onset. Mean concentrations of all of the hormones measured exhibited significant changes (P<0·01) with date of sampling. Overall mean concentrations of insulin, tri-iodothyronine and thyroxine did not differ with treatment but, compared with L animals, H animals exhibited higher mean concentrations of prolactin in April and May (P<0·05) and of insulin-like growth factor-1 in December and January (P<0·001). Rates of activity of MDII and MDIII in skin differed with date (P<0·001) but were not significantly affected by nutritional treatment. The MDIII/MDII ratio differed (P=0·05) with month but was significantly higher (P<0·05) in L than H animals in January, only. It is concluded that the reduction in hair follicle activity and the slower onset of moult associated with reduced nutrition were unlikely to be controlled, directly, by differences in activities of MDII or MDIII in skin tissue.