Sequential Pathophysiologic Effects of Ionizing Radiation on the Beagle Thyroid Gland

Summary

Response of the thyroid gland to ionizing radiation exposure manifested itself over time: a) functionally by transient increased activity and progressive hypothyroidism and b) pathologically by degeneration, hyperplasia, and carcinogenesis. Although such phenomena were described in animals and man, the pathogenesis and mechanism of the reaction have not been elucidated. We studied dogs to obtain evidence of some factors which may initiate and amplify the visible and functional thyroid derangement. Increase in circulating TSH seemed secondary to the glandular damage. Thyroid-stimulating hormone also seemed to promote the progressive change, its self-perpetuation, and the sequence of events leading to permanent hyperplasia or carcinogenesis. The postirradiation latency for induction of thyroid neoplasia in dog (4-10 yr), man (9-14 yr), and rat (1-2 yr) showed a linear relationship with basal metabolic rate. Although this relationship might have been fortuitous, it could have indicated a fundamental connection tissue metabolism and thyroid cell turnover rate.