Linked Life Data

3591538

Source:http://linkedlifedata.com/resource/pubmed/id/3591538

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1987-6-26
pubmed:abstractText
Iodine is an essential nutrient for the normal growth and development of humans and animals and is necessary for normal metabolism and regulation of thyroid hormones. Iodine excess can produce thyrotoxicosis but not cancer. However, radioiodine is carcinogenic for the thyroid gland. Dietary iodine deficiency is associated with goiter in humans and animals. The goiter develops because of a feedback system between thyroid hormones, the pituitary gland, and the hypothalamus, and it regulates the synthesis and release of thyroid-stimulating hormone. Chronic hypersecretion of thyroid-stimulating hormone causes profound goiter (diffuse thyroid hyperplasia), which appears to be related to carcinogenesis. Chronic dietary iodine deficiency in rats leads to thyroid follicular adenomas by 12 months and follicular carcinomas by 18 months. An increased risk of thyroid cancer has been reported in humans with goiter and those living in some iodine-deficient areas of the world. In very recent animal studies, iodine deficiency, chemical goitrogens, and thyroid toxins have been shown to have potent tumor-promoting effects. In rats, iodine deficiency is a much more effective tumor promoter than it is a carcinogen, suggesting that a similar relationship may exist in human populations. These studies suggest that a major role of iodine is to prevent the formation of thyroid tumors in humans and animals.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0065-2598
pubmed:author
pubmed:issnType
Print
pubmed:volume
206
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
529-42
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1986
pubmed:articleTitle
The role of iodine in carcinogenesis.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.