title: Iodine toxicity and its amelioration.
abstract: Iodine (I) toxicity is rare in animals and humans, but nuclear explosions that give off radioactive I and excessive stable I ingestion in parts of the world where seaweed is consumed represent specialized I toxicity concerns. Chronic overconsumption of I reduces organic binding of I by the thyroid gland, which results in hypothyroidism and goiter. Bromine can replace I on position 5 of both T(3) and T(4) with no loss of thyroid hormone activity. Avian work has also demonstrated that oral bromide salts can reverse the malaise and growth depressions caused by high doses of I (as KI) added as supplements to the diet. Newborn infants by virtue of having immature thyroid glands are most susceptible to I toxicity, whether of stable or radioactive origin. For the latter, the 1986 Chernobyl nuclear accident in Belarus has provided evidence that KI blockage therapy for exposed individuals 18 years of age and younger is effective in minimizing the development of thyroid cancer. Whether bromide therapy has a place in I toxicity situations remains to be determined.
authors.affiliation: Department of Animal Sciences and Division of Nutritional Sciences, 290 Animal Sciences Laboratory, University of Illinois, 1207 West Gregory Drive, Urbana, Illinois 61801, USA. dhbaker@uiuc.edu
authors.forename: David H
authors.initials: DH
authors.lastname: Baker
mesh_terms: D000818:Animals; D000931:Antidotes / Q000627:therapeutic use*; D001965:Bromides / Q000627:therapeutic use; D006801:Humans; D007455:Iodine / Q000506:poisoning*; D007457:Iodine Radioisotopes / Q000506:poisoning; D011041:Poisoning / Q000188:drug therapy / Q000209:etiology
chemical_list: D000931:Antidotes; D001965:Bromides; D007457:Iodine Radioisotopes; D007455:Iodine