Thyroidal iodine metabolism in obese-strain chickens before immune-mediated damage.

Several studies have shown that iodine plays a role in spontaneous autoimmune thyroiditis in man and other animals. In addition, abnormalities of iodine metabolism have been found in patients with Hashimoto's thyroiditis and in chickens of the obese strain (OS), an animal model of spontaneous autoimmune thyroiditis. We have examined several parameters of iodine metabolism before immune damage in this model and in the related Cornell strain (CS), a strain which develops a late-onset mild thyroiditis, to discover a possible causal relationship between altered iodine metabolism and the initiation of autoimmunity.

Antioxidants delay the onset of thyroiditis in obese strain chickens.

Dietary iodine has been shown to be important in the induction of thyroiditis in susceptible chicken strains although the underlying mechanism remains unknown. Iodine may exert its effects through the formation of reactive oxidative radicals which would cause thyroidal injury and initiate infiltration. We have tested this hypothesis by examining the ability of butylated hydroxyanisole (BHA), ethoxyquin, and other antioxidants to prevent thyroiditis in Obese strain (OS) chickens, a strain that develops severe disease by 4 weeks of age.

The incorporation of dietary iodine into thyroglobulin increases its immunogenicity.

Experiments were performed to analyze one mechanism by which elevated levels of dietary iodine may induce thyroglobulin (Tg) autoantibodies. We tested the hypothesis that highly iodinated Tg synthesized by animals fed a high iodine diet is significantly more immunogenic than Tg containing fewer iodine atoms. Cornell strain (CS) chickens, genetically susceptible to iodide-induced thyroiditis, were fed either a high or a low iodine diet.