Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2002-6-14
pubmed:abstractText
There has been growing concern about the potential threat of hormone-disrupting chemicals like bisphenol A to various aspects of animal and human health. We studied the effects of bisphenol A on the Cl(-) secretion in human airway epithelial Calu-3 cells. Pretreatment with bisphenol A (IC(50) = 60 microM, for 30 min) prevented isoproterenol (10 nM)-generated short-circuit current (I(sc)) more potently than 17beta-estradiol or tamoxifen (IC(50) = 1 mM). 5'-Nitro-2-(3-phenylpropylamino) benzoate-sensitive apical conductance potentiated by isoproterenol was not affected by the pretreatment with either of these estrogenic compounds. The effects of bisphenol A were simulated in I(sc) responses to forskolin (10 microM) and 8-bromo-cAMP (1 mM). Nystatin permeabilization of Calu-3 monolayers revealed that bisphenol A attenuated 8-bromo-cAMP-induced basolateral K+ current, which is sensitive to clotrimazole (30 microM) and insensitive to charybdotoxin (100 nM), without affecting the apical Cl(-) current. Bisphenol A, but neither 17beta-estradiol nor tamoxifen, interrupted the charybdotoxin-sensitive component of I(sc) stimulated by 1-ethyl-2-benzimidazolinone (1-EBIO; 500 microM). The inhibitory effects of bisphenol A on these Cl(-) secretory stimuli were remarkable when applied to the apical rather than the basolateral membrane. Alternatively, long-term incubation of bisphenol A (1 microM; 12-72 h) had no discernible effect on isoproterenol- and 1-EBIO-induced Cl(-) secretion. These findings indicate that short-term exposure to bisphenol A attenuates transepithelial Cl(-) secretion through inhibition of both cAMP- and Ca(2+)-activated K+ channels on the basolateral membrane, interacting from the cytosolic surface in Calu-3 cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/1-ethyl-2-benzimidazolinone, http://linkedlifedata.com/resource/pubmed/chemical/Adrenergic beta-Agonists, http://linkedlifedata.com/resource/pubmed/chemical/Benzimidazoles, http://linkedlifedata.com/resource/pubmed/chemical/CFTR protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Chloride Channels, http://linkedlifedata.com/resource/pubmed/chemical/Chlorides, http://linkedlifedata.com/resource/pubmed/chemical/Cyclic AMP, http://linkedlifedata.com/resource/pubmed/chemical/Cystic Fibrosis Transmembrane..., http://linkedlifedata.com/resource/pubmed/chemical/Isoproterenol, http://linkedlifedata.com/resource/pubmed/chemical/Phenols, http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channel Blockers, http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channels, http://linkedlifedata.com/resource/pubmed/chemical/bisphenol A
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0022-3565
pubmed:author
pubmed:issnType
Print
pubmed:volume
302
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
80-7
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
Bisphenol A inhibits Cl(-) secretion by inhibition of basolateral K+ conductance in human airway epithelial cells.
pubmed:affiliation
Division II (Respiratory Division), Internal Medicine II, University of Nagoya School of Medicine, Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't