Vascularization and iodide transport down regulation in rat goitre

Abstract

Abstract. This study was designed to investigate, in the rat, the regulation of the amount of thyroid iodide and of its organification during the involution of an experimentally induced goitre. The goitre was obtained by drastic iodine deficiency; male Wistar rats received an iodide deficient diet for 6 months, supplemented with PTU during the last 2 months. The study was followed for 16 days after the beginning of iodide refeeding (daily iodine intake = 50 μg). The thyroid iodide, total thyroid organic iodine and plasma iodide, PBI and TSH concentrations were determined from day 0 to 16 and compared to their control values (rats on a normal iodide diet for 6 months). In addition, a stereological study was carried out to determine if the extent of the gland vasculature might be implicated in the regulation of the thyroid iodide content. The plasma TSH concentration was very high and constant for 8 days (2.40 ± 0.37 and 2.45 ± 0.43 on day 0 and 8 respectively vs 0.25 ± 0.12 μg/ml in control rats), whereas iodination and secretion were blocked for 4 days (0.34 ± 0.19 and 0.5 ± 0.1 on day 0 and 4 respectively vs 14.4 ± 2.0 μg 127I/gland in control rats) (Wolff-Chaikoff effect). Thyroid iodide amount increased enormously for 2 days (2.5 ± 0.6 and 2.45 ± 0.55 respectively on day 1 and 2 vs 0.09 ± 0.01 μg 127I/gland on day 0), then strongly decreased between 2 and 4 days (1.15 ± 0.27 127I/gland). The thyroid/serum (T/S) ratio (iodide pump), which was very important between 0 and 2 days (115), decreased strikingly on day 4 (55). Moreover, the thyroid homogenates were shown to contain a new (nonproteic) iodocompound which escaped classical iodination. Its mobility during polyacrylamide gel electrophoresis was intermediary between those of iodoaminoacids and iodide. Its turnover rate was practically similar to that of thyroid iodide. This compound (termed 'X') accumulated until day 2 (0.39 ± 0.03 μg 127I/gland), then decreased sharply as did thyroid iodide, whereas neoiodination resumed (Wolff-Chaikoff escape). The stereological results showed that as soon as the iodide refeeding started, the volume density as well as the surface density of vessels sharply decreased (0.23 ± 0.03 μm3/μm3 and 0.06 ± 0.03 μm2/μm3 on day 0 and 8, respectively), whereas the same parameters for thyroid epithelial cells remained constant (0.35 ± 0.02 μm3/μm3 and 0.32 ± 0.03 μm2/μm3 on day 0 and 8, respectively. From these data we can conclude that a great iodide influx in hyperstimulated thyroid epithelial cells induces a cellular control, antagonist to the TSH action on the amount of thyroid iodide. This control acts sequentially: an early regression of the thyroid vasculature is observed, which is followed by a regulation of iodide active transport. The 'X' iodocompound might be one of the factors implicated in this control.