ABSTRACT
Previous in vivo studies in mice have shown that polyphloretin phosphate (PPP), a polyionic polyester of phosphoric acid and the dihydrochalcone phloretin, can inhibit thyroid hormone secretion induced by TSH and by the long-acting thyroid stimulator of Graves' disease (LATS), but not that induced by catecholamines or 5-hydroxytryptamine (5-HT). The present study was undertaken to explore further the mechanism of this effect, particularly the possibility that PPP interferes with the synthesis of endogenous prostaglandins (PG). Therefore, the effects of PPP and some of its subfractions and congeners were compared with those of indomethacin, a known inhibitor of PG synthesis, with respect to their influence on the blood radioiodine (BRI) increase in response to TSH, 5-HT, and isoprenaline (IPNE) in 125I- and T4-pre-treated mice.
When given alone, neither indomethacin nor PPP or its subfractions reduced the BRI levels. Instead, small increments were seen in occasional experiments. Indomethacin did not inhibit the BRI increase in response to any of the thyroid-stimulating agents, but rather enhanced the responses in occasional experiments. PPP and some of its high-molecular weight subfractions reduced the BRI increases in response to TSH but not those to 5-HT or IPNE. The findings do not support the concept that de novo synthetized PG mediates TSH activation of thyroid hormone secretion, but they favour the view that PPP inhibits the action of TSH at its receptor site.
Serum long acting thyroid stimulator protector in pregnancy complicated by Graves' disease.