Abstract
Iodine is one of the essential micronutrient which is required for the synthesis of thyroid hormones. Thus, iodine deficiency may result in the hypothyroidism. Iodine deficiency is one of the most common causes of preventable mental retardation and brain damage in the world. On the other hand, Japanese iodine intake exceeds that of most other countries, due to the significant seaweed consumption such as kelp. The Japanese Ministry of Health, Labour and Welfare estimates average iodine consumption at 1.2mg/day in Japan. In contrast, the recommended tolerable upper intake levels for adult is 1.1 mg / day in the United States. Generally, Japanese takes twenty times higher amount of iodine than Americans. Iodine tolerance among individual humans varies greatly, and the excess iodine can cause both hyper- and hypo- thyroidism. Furthermore, the effect of thyroid dysfunction due to iodine excess on brain function has not been clarified. In this study, we generated a mouse models for chronic iodine excess and evaluated its effect on brain development. C57BL/6 dams and their pups mice were treated with KIO3 37.4mg/l through drinking water. Behavioral experiments (novel object recognition test, novel object in location test, visual discrimination test, and three-room social behavior test) were conducted at 10-weeks-old. After the behavioral analysis, mice were sacrificed to collect trunk blood and tissues. Excess iodine intake caused hypertrophy of thyroid follicles regardless of the administered dose. However, there were no differences in thyroid hormone status among groups. Thyroid hormone responsive genes in the hippocampus were also not affected in experiment group. In the behavioral analysis, female mice showed an increase in learning ability. In summary, although the chronic overdose of iodine does not affect thyroid hormone levels, it may affect cognitive learning function. The gender difference in the consequence was also observed. These results indicate that the chronic iodine excess may cause various changes, although the body is tolerable with excess iodine.
Thyroid dysfunction is associated with the loss of hepatitis B surface antigen in patients with chronic hepatitis B undergoing treatment with α-interferon
