THE POSTNATAL SERUM 3,5,3'-TRIIODOTHYRONINE (T(3)) SURGE IN THE RAT IS LARGELY INDEPENDENT OF EXTRATHYROIDAL 5'-DEIODINATION OF THYROXINE TO T(3)

In the rat, selenium deficiency causes a near-complete loss of the sel enoenzyme type I 5'-deiodinase (5'D-I), resulting in a marked decrease in hepatic T4 to T3 conversion. In adult rats, serum T4 concentration s are consistently increased, whereas serum T3 and rT3 concentrations are unaffected or slightly decreased and increased, respectively. In r at fetuses near term, serum T4 and rT3 concentrations are not affected by selenium deficiency. We have now studied the effect of selenium de ficiency on thyroid function in the neonatal rat. Weanling female rats were fed either a selenium-supplemented or a selenium-deficient diet for 4 weeks before mating and then throughout gestation and lactation. Neonatal rats were killed at 7, 14, 21, and 28 days. Selenium deficie ncy was confirmed by a more than 89% decrease in liver 5'D-I activity in mothers and pups. Selenium deficiency resulted in significant incre ases in serum T4 concentrations in 3- and 4-week-old pups. In contrast , selenium deficiency led to a striking increase in serum rT3 concentr ations. The normal postnatal serum Ta surge was not affected by seleni um deficiency at any age. In 2- and 4-week-old selenium-deficient pups obtained from a second litter from the same mothers, liver 5'D-I acti vity was markedly decreased, but thyroid 5'D-I activity was not affect ed. The increased serum rT3 and, less so, T, concentrations observed i n selenium-deficient pups were associated with a significant decrease in brain 5'D-II activity in 14- and 28-day-old pups and in brown adipo se tissue 5'D-II activity in 14-day-old pups. In conclusion, the prese nt study demonstrates that the increase in serum T4 concentrations con sistently observed in selenium-deficient adult rats occurs only after the second week of life. The normal physiological postnatal 12-fold in crease in serum T3 concentrations observed in selenium-deficient pups despite the marked decreases in liver 5'D-I and brain and brown adipos e tissue 5'D-II activities suggests that T4 to T3 conversion by periph eral tissues may not be a major source of T3 in the neonate. In contra st, the thyroid gland, whose 5'D-I activity is not affected by seleniu m deficiency, is probably the principal source of circulating T3 in th e neonate. Finally, the early and marked increase in serum rT3 concent rations observed in selenium-deficient pups suggests that liver 5'D-I is important in rT3 deiodination.