129I and 137Cs fission products in thyroids of animals, 1984-1991.

Iodine is intensely concentrated in the thyroid of animals, while 137Cs is not. In this study, 129I and 137Cs concentrations were determined in animal thyroids from selected areas during 1984-1991. The thyroids were from deer killed within the Savannah River Site (SRS) in South Carolina; from the environs of Oak Ridge (OR), Tennessee; West Tennessee; and Florida. Thyroids from sheep slaughtered routinely in Birmingham, England (UK), were also tested. The glands were analyzed by x-ray spectroscopy using a high-purity germanium well detector. 129I concentrations of 1 to 102 Bq 129I (g thyroid)-1 were found in 6.8% of deer thyroids from SRS. Eighty-nine percent of the thyroids from SRS and 38% of those from OR contained 129I concentrations of 0.01 to 1.0 Bq 129I g-1. No thyroids from West Tennessee or Florida had more than 4 mBq 129I g-1. Cesium was found to be distributed differently; 38% of the thyroids from SRS contained 0.1 to 0.65 Bq 137Cs g-1, and the highest concentrations appeared periodically, during November and December. Ten to 100 mBq of 137Cs were found in 60% of thyroids from SRS, 79% of those from Florida, 52% of those from OR, and 22% of those from West Tennessee. In thyroids from SRS and Florida, most of the 137Cs has been from worldwide fallout on sandy soil which permits 137Cs-rich vegetation; if a fraction of the 137Cs is from other sources, it has not been defined. The unique finding of this report is the high incidence and persistence of > 0.01 Bq 129I (g thyroid)-1 in deer from OR and SRS. 129I is a marker for fission products, but it is not a radiological hazard because of its very slow radioactive decay and its continual dilution by additions of nonradioactive iodine to the environment.

T-2 mycotoxin intensifies iodine deficiency in mice fed low iodine diet.

Mice were depleted of iodine and fed a 125I-labeled low iodine diet. After they developed isotopic equilibrium they were given T-2 mycotoxin, in doses 34% to 14% of LD50/day for 4 to 12 days. In all cases T-2 toxin caused loss of thyroid iodine from which the animals recovered when the T-2 toxin was stopped. When iodine intake was adequate, the T-2 toxin had no statistically significant effect on the thyroid iodine content. Since T-2 toxin is known to block the initiation of some protein synthesis, it may block thyroglobulin synthesis, and, in stimulated thyroids, limited hydrolysis may continue. Therefore, when the thyroids were stimulated and thyroglobulin was depleted, a blockade of thyroglobulin synthesis may have caused further depletion of thyroidal iodine.

Biologically available iodine in goitrogenic diets.

Eight different sources of low-iodine diet (LID) were tested in mice over 14 years. The available iodine in each diet was measured by isotopic equilibration. Commercially prepared Remington diets contained 6.8 to 69.3 ng available iodine/g, and the results were usually different from shipment to shipment. Some samples produced greatly enlarged thyroids. The Remington diets from two sources were occasionally low in iodine but produced little thyroid enlargement. Between 1977 and 1980 only one shipment of Remington diet was found to contain less than 10 ng available I/g, and it resulted in large goiters. Since 1980 other compositions of LID have been used, but they caused additional abnormalities during breeding or chronic feeding. A low-iodine wheat diet produced goiter in mice more readily than in rats. In the course of testing for unavailable forms of dietary iodine, it was found that only 34.2% of thyroxine iodine was available to the thyroid iodine pool of mice. It is concluded that unidentified nutritional deficiency or dietary contaminants can alter the goitrogenic response to restricted iodine intake. Furthermore, at least one natural form of potential dietary iodine is incompletely available to mice.

Thiocyanate feeding with low iodine diet causes chronic iodine retention in thyroids of mice.

Effects of KSCN on thyroidal iodine metabolism were studied in weanling mice fed a low iodide diet (LID) labeled continuously with 125I as iodide. The addition of KSCN (0.3 and 0.6 mg/g diet) resulted in the accumulation of an unusual iodinated protein within the follicles of the mouse thyroids. After 60 days, total thyroidal iodine was 4 times greater than in controls without thiocyanate. The iodinated protein was essentially insoluble at pH 8.0 and was very slowly released from the thyroids; it contained more MIT than DIT and little thyroid hormone. By use of three isotopes (125I, 127I, and 131I) and auto-radiographs, there were shown different iodinated proteins synthesized during high and low iodine intakes and coexistent but segregated in the colloid. Low doses of perchlorate or iodide inhibited or prevented accumulation of the essentially insoluble iodinated protein. It is suggested that when mouse thyroids are iodine depleted, thiocyanate increases the formation of an essentially insoluble iodinated thyroglobulin within the thyroid. Only a small fraction of the iodination may have occurred by this route, but the rate of formation exceeded the rate of release, so the product continuously accumulated.

The use of iodine as a thyroidal blocking agent in the event of a reactor accident. Report of the Environmental Hazards Committee of the American Thyroid Association.

In the event of a nuclear reactor accident, radioactive materials could be released into the environment: radioisotopes of iodine could constitute a major component of such a release. Upon such exposure, radioiodines could enter the body and accumulate in an unprotected thyroid gland where they would remain for varying periods of time. A number of methods have been proposed to protect those at risk of exposure. Administration of thyroid-blocking agents (such as potassium iodide) to exposed populations could be effective, but their use has raised a number of questions since there are considerable gaps in the scientific information available about the possible effects of low-level radiation from radioiodine. In addition, there are only limited data available about potential toxic side effects of potassium iodide distributed widely to large, unsupervised populations. Concern about these issues led the American Thyroid Association to appoint a committee of its members with special interest and competence in these areas to review the problems in detail and develop an advisory statement on the questions at issue for those to whom this matter might be of concern.

Immunoreactive somatostatin and beta-endorphin content in the brain of mature rats after neonatal exposure to propylthiouracil.

The contents of immunoreactive somatostatin (IR-SRIF) and beta-endorphin (IR-beta-EP) in 12 brain regions were examined in rats exposed neonatally to propylthiouracil (PTU) through the mother's milk. Since the dose of PTU used in this study is lower than the usual dose employed to induce hypothyroidism, a milder form of neonatal hypothyroidism resulted. This conclusion is supported by the only mild subnormal growth of rats to adulthood and serum T4 and T3 concentrations in the normal range. Adult rats treated with PTU neonatally had significantly higher IR-SRIF contents in several brain regions compared to controls, whereas IR-beta-EP levels were not significantly different (significant increase only in the thalamus) in most regions. The results indicate that even mild hypothyroidism during early postnatal development causes permanent impairment of brain function, which manifests itself in part by an altered brain content of IR-SRIF.

Audiogenic seizures and cochlear damage in rats after perinatal antithyroid treatment.

The feeding of goitrogens during pregnancy and lactation causes the offspring of rats to be partially deaf and persistently sensitive to audiogenic seizures. The most potent goitrogen, propylthiouracil, caused severe dysfunction and disorganization of the organ of Corti. Adult seizure-susceptible rats showed increased sensitivity to audiogenic seizures when they were fed propylthiouracil.