Vulnerability of the developing brain to thyroid abnormalities: environmental insults to the thyroid system.

Hdl Handle:
http://hdl.handle.net/10675.2/113
Title:
Vulnerability of the developing brain to thyroid abnormalities: environmental insults to the thyroid system.
Authors:
Porterfield, S P
Abstract:
Neurologic development follows orderly patterns that can be severely disturbed when thyroid hormones are deficient or excessive. Should this occur at appropriate development periods, irreversible neurologic damage can result. The nature of the deficits depends upon the specific development period and the severity of the thyroid disturbance. PCBs and dioxins are structurally similar to the thyroid hormones. Their binding characteristics are similar to those of thyroid hormones and all three groups bind to the cytosolic Ah receptor, the thyroid hormone receptor and the serum thyroid hormone binding protein transthyretin. Depending upon the dose of toxin and the congener used, the toxins either decrease or mimic the biological action of the thyroid hormones. Either effect, if occurring during brain development, can have disastrous consequences. Children and animals exposed to PCBs or dioxins in utero and/or as infants can exhibit varying degrees of behavioral disorders. These disorders resemble those seen in children exposed to thyroid hormone deficiencies in utero and/or in infancy. The mechanism of developmental neurotoxicity of PCBs and dioxins is not known but data suggest it could be partially or entirely mediated by alterations in availability and action of thyroid hormones during neurological development. It is possible that transient exposure of the mother to doses of toxins presently considered nontoxic to the mother could have an impact upon fetal or perinatal neurological development. If the toxins act via their effect on thyroid hormone action, it is possible that doses of toxins that would normally not alter fetal development, could become deleterious if superimposed on a pre-existing maternal/or fetal thyroid disorder.
Citation:
Environ Health Perspect. 1994 Jun; 102(Suppl 2):125-130
Issue Date:
23-Nov-1994
URI:
http://hdl.handle.net/10675.2/113
PubMed ID:
7925183
PubMed Central ID:
PMC1567088
Type:
Journal Article; Review
ISSN:
0091-6765
Appears in Collections:
Department of Physiology: Faculty Research and Presentations

Full metadata record

DC FieldValue Language
dc.contributor.authorPorterfield, S Pen_US
dc.date.accessioned2010-09-24T22:03:22Z-
dc.date.available2010-09-24T22:03:22Z-
dc.date.issued1994-11-23en_US
dc.identifier.citationEnviron Health Perspect. 1994 Jun; 102(Suppl 2):125-130en_US
dc.identifier.issn0091-6765en_US
dc.identifier.pmid7925183en_US
dc.identifier.urihttp://hdl.handle.net/10675.2/113-
dc.description.abstractNeurologic development follows orderly patterns that can be severely disturbed when thyroid hormones are deficient or excessive. Should this occur at appropriate development periods, irreversible neurologic damage can result. The nature of the deficits depends upon the specific development period and the severity of the thyroid disturbance. PCBs and dioxins are structurally similar to the thyroid hormones. Their binding characteristics are similar to those of thyroid hormones and all three groups bind to the cytosolic Ah receptor, the thyroid hormone receptor and the serum thyroid hormone binding protein transthyretin. Depending upon the dose of toxin and the congener used, the toxins either decrease or mimic the biological action of the thyroid hormones. Either effect, if occurring during brain development, can have disastrous consequences. Children and animals exposed to PCBs or dioxins in utero and/or as infants can exhibit varying degrees of behavioral disorders. These disorders resemble those seen in children exposed to thyroid hormone deficiencies in utero and/or in infancy. The mechanism of developmental neurotoxicity of PCBs and dioxins is not known but data suggest it could be partially or entirely mediated by alterations in availability and action of thyroid hormones during neurological development. It is possible that transient exposure of the mother to doses of toxins presently considered nontoxic to the mother could have an impact upon fetal or perinatal neurological development. If the toxins act via their effect on thyroid hormone action, it is possible that doses of toxins that would normally not alter fetal development, could become deleterious if superimposed on a pre-existing maternal/or fetal thyroid disorder.en_US
dc.rightsThe PMC Open Access Subset is a relatively small part of the total collection of articles in PMC. Articles in the PMC Open Access Subset are still protected by copyright, but are made available under a Creative Commons or similar license that generally allows more liberal redistribution and reuse than a traditional copyrighted work. Please refer to the license statement in each article for specific terms of use. The license terms are not identical for all articles in this subset.en_US
dc.subject.meshAnimalsen_US
dc.subject.meshBrain / embryology / growth & developmenten_US
dc.subject.meshCongenital Hypothyroidismen_US
dc.subject.meshEmbryonic and Fetal Developmenten_US
dc.subject.meshEnvironmental Exposure / adverse effectsen_US
dc.subject.meshFemaleen_US
dc.subject.meshHumansen_US
dc.subject.meshHypothyroidism / complicationsen_US
dc.subject.meshPregnancyen_US
dc.subject.meshPregnancy Complicationsen_US
dc.subject.meshPrenatal Exposure Delayed Effectsen_US
dc.subject.meshThyroid Hormones / physiologyen_US
dc.titleVulnerability of the developing brain to thyroid abnormalities: environmental insults to the thyroid system.en_US
dc.typeJournal Articleen_US
dc.typeReviewen_US
dc.identifier.pmcidPMC1567088en_US
dc.contributor.corporatenameDepartment of Physiologyen_US

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