Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2006-8-2
pubmed:abstractText
2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is among the most toxic pollutants known to date that serves as a prototype for a group of halogenated hydrocarbon compounds characterized by extraordinary environmental persistence and unique ability to concentrate in animal and human tissues. TCDD can elicit a complex array of pleiotropic adverse effects in humans, although chloracne, a specific type of acne-like skin disease, is the only consistent manifestation of dioxin intoxication, thus representing a 'hallmark' of TCDD exposure. Chloracne is considered to be one of the most specific and sensitive biomarkers of TCDD intoxication that allows clinical and epidemiological evaluation of exposure level at threshold doses. The specific cellular and molecular mechanisms involved in pathogenesis of chloracne are still unknown. In this review, we summarize the available clinical data on chloracne and recent progress in understanding the role of the dioxin-dependent pathway in the control of gene transcription and discuss molecular and cellular events potentially involved in chloracne pathogenesis. We propose that the dioxin-induced activation of skin stem cells and a shift in differentiation commitment of their progeny may represent a major mechanism of chloracne development.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0906-6705
pubmed:author
pubmed:issnType
Print
pubmed:volume
15
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
705-30
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Dioxin-induced chloracne--reconstructing the cellular and molecular mechanisms of a classic environmental disease.
pubmed:affiliation
Department of Dermatology, Columbia University, New York, NY 10032, USA. ap374@columbia.edu
pubmed:publicationType
Journal Article, Review