Effect of X-Irradiation on the Thyroid Gland of Beagles Fed a Restricted Iodide Diet

• Published in: Radiation research 1972-08, Vol.51 (2), p.333-360
• Main Authors: Fritz, T. E., Norris, W. P., Taylor, J. A., Kretz, N. D.
• Format: Article
• Language: English
• Subjects: Animals; Autoradiography; Colloids; Diet; Dogs; Epithelium; Female; Half-Life; Histology; Hyperplasia; Iodides; Iodides - metabolism; Iodine Isotopes; Male; Organ Size; Radiation damage; Radiation dosage; Radiation Effects; Thyroid gland; Thyroid Gland - anatomy & histology; Thyroid Gland - metabolism; Thyroid Gland - pathology; Thyroid Gland - radiation effects; Thyroidectomy; Time Factors
• ISSN: 0033-7587; 1938-5404
• DOI: 10.2307/3573614

When the usual iodide intake of beagles was reduced to 50-75 μg/day, their thyroid glands responded by cellular hyperplasia and hypertrophy, loss of colloid, and increased glandular weight. After about 1 year, the enlarged thyroid glands had accommodated to reduced dietary iodine and presented a normal histologic appearance. When both thyroid lobes of similarly fed beagles were exposed to 2000 R of 250 kVcp x-rays, there was cellular hypertrophy and loss of colloid, but cellular hyperplasia and increased glandular size and weight did not occur. The irradiated glands did not regain a normal histologic appearance, but became fibrotic. If only one lobe of the thyroid was irradiated, the irradiated lobe became fibrotic, while the unirradiated lobe responded to the change in iodine intake as if neither lobe had been irradiated. When the enlarged unirradiated lobe had reverted to a more normal histologic appearance, the irradiated gland responded similarly, but was not increased in size. All histologic changes correlated wth changes in iodide metabolism, measured by repeated tests using 131 I. Hyperplastic glands accumulated large fractions of tracer doses of 131 I, but released iodine more rapidly than did normal-appearing glands. The reversion of such hyperplastic glands to a normal histologic appearance was characterized by an abrupt decrease in the rate of release of 131 I, with 131 I uptake remaining high. Exposure to 2000 R completely destroys the proliferative capability of thyroid cells but does not prevent the original, irradiated cells from reacting to stimuli for increased thyroid function.