Preincubation of canine thyroid slices in KRP for 1–2 hr increased the organic binding of iodine by such slices and their response to TSH and other stimulators of iodination. TSH, dibutyryl cyclic 3′,5 ′-AMP (dbcAMP), NaF and prostaglandin Ei (PGE1) each stimulated organic binding of iodine and formation of thyroxine in preincubated slices and their effects were not additive. Anti-TSH rabbit serum blocked the effect of TSH on organisation, but not the effect of dbcAMP. Stimulation of organic binding by TSH, dbcAMP, NaF and PGE1 was still apparent in the presence of perchlorate. The presence of hydrogen peroxide in the medium enhanced organic binding of iodide and thyroxine formation in thyroid slices and this effect was not additive with the effects of TSH, dbcAMP, NaF or PGE1. Under conditions where organic binding by slices was blocked, T/M radioiodine concentration ratios after 30 min and 6 hr incubation periods were lower than controls in the presence of TSH, dbcAMP, NaF and PGE1. Adenyl cyclase activity of canine thyroid homogenate was stimulated by TSH, NaF and PGE1. TSH and PGE1, but not NaF, enhanced the incorporation of radiocarbon derived from 8-14Cadenine into cyclic 3′,5′-AMP of canine thyroid slices. These results suggest that the stimulation of organic binding of iodine by TSH and PGE1 is probably mediated through increased formation of cyclic 3′,5′-AMP, while augmented organic binding secondary to F− may involve other mechanisms. Enhanced formation or availability of H2O2 could be a common factor in the enhanced organic binding observed in the presence of fluoride and PGE1 as well as TSH and dbcAMP. (Endocrinology86: 396, 1970)
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AHN et al. (1970) studied this question.