The effects of the daily feeding of 6 μg of propylthiouracil1/rat for about two weeks on the thyroid of animals maintained on different levels of iodine intake (from 0.5–3.6 μg/day/100 g BW) have been investigated. We have confirmed previous observations by other authors (Yamada & Schichijo 1962; Greer et al. 1962) showing that very low doses of PTU increase thyroid weight in rats on a low iodine supply without necessarily decreasing their rather low plasma PBI or their high thyroidal 131I uptake, and that the same doses no longer have an effect on thyroid weight if the iodine intake is raised. In the present experiments this occurred when the iodine intake was raised to about 1.2–1.3 μg/day/100 g BW. As shown here, it is unlikely that these low doses of PTU block synthesis of the thyroid hormones. They do, however, slightly inhibit the extrathyroidal deiodination of T4 and they probably trigger thyrotrophin (TSH) release from the pituitary gland. The present findings are compatible with the view that very small doses of PTU can be goitrogenic if the rats are on an iodine intake which is barely adequate for normal peripheral requirements, because these are increased chronically, even if slightly. Because of the low iodine stores the thyroid would then be unable to compensate for these increased hormone requirements. Even a small increase of available iodine may avoid this situation so that the effects of the low PTU doses are no longer detectable either in the plasma TSH activity or in the thyroid weight. The low PTU doses used here appear to hasten and aggravate a situation which would eventually develop from a more prolonged or a more severe degree of iodine deficiency only. The experimental situation induced by these low PTU doses might serve as an interesting model system for the study of simple goitre in areas in which iodine deficiency is not too extreme.