Autoregulation of iodide transport in the rabbit: absence of autoregulation in fetal tissue and comparison of maternal and fetal thyroid iodination products.

Abstract

Maternal and fetal rabbit thyroid glands were compared as to their ability to respond to excess iodide in vitro with a reduction in subsequent iodide transport activity. Preincubation of maternal thyroid tissue slices for 2 h with excess iodide (30 microM) resulted in a 31% reduction in the subsequently measured thyroid-medium radioiodide concentration ratio. In contrast, similar iodide pretreatment had no significant effect on fetal iodide transport. In all other respects, fetal iodide transport, although it was 10 times higher, did not differ significantly from maternal transport activity. Combined radiolabeled maternal (125I) and fetal (131I) rabbit thyroid tissue was eluted on Sephadex G-25 columns. Fractions were analyzed for both 125I and 131I activity, and the maternal to fetal ratios (125I/131I) were determined for each fraction. The majority of iodoproteins eluted with the void volume, and the 125I/131I ratio was constant in these fractions. Thereafter, two peaks of elevated 125I/131I activity could be observed. Peak A eluted below lysozyme (Mr = 14,300) and above insulin (Mr = 6,000), with an apparent mol wt of 8,000 to 10,000. A second peak, peak B, eluted from the column at a site similar to that of MIT or a protein of Mr of 2,000. Ascending paper chromatography of this latter peak of 125I/131I activity and MIT was carried out in two solvent systems. In both systems, peak B comigrated with MIT. These findings suggest that the failure of fetal thyroid tissue to exhibit autoregulation may be associated with the reduced iodination of a compound with an approximate Mr of 8,000 to 10,000. The role of this substance in iodide transport remains to be identified. The reason for the apparent increase in the labeling of MIT observed in maternal vs. fetal tissue is unknown.