Source:http://linkedlifedata.com/resource/pubmed/id/10373400
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
1999-7-12
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pubmed:abstractText |
Some environmental chemicals exhibit estrogenic or antiandrogenic activity. Some of these, such as bisphenol A (bis A) and octylphenols, are used in large amounts in many applications. We have analyzed the effects of bis A and octylphenols on steroidogenesis in Leydig cells by measuring the LH receptor-mediated cAMP and progesterone (P) production in cultured mouse Leydig tumor cells (mLTC-1 cells). After preincubation of mLTC-1 cells for 48 h in the presence of bis A or one of the octylphenols in micromolar concentration, the hCG-stimulated cAMP and P formation in these cells was inhibited. Bis A or octylphenols could neither inhibit cAMP nor P formation stimulated by forskolin (Fk) or cholera toxin (CT) nor steroidogenesis stimulated by 8-Br-cAMP. The preincubation of mLTC-1 cells with estradiol or diethylstilbesterol (DES) at the concentration of 10(-8) mol/liter had no inhibitory effect on cAMP formation stimulated by hCG or Fk but P production was inhibited. Similarly, both estrogens inhibited P production stimulated by 8-Br-cAMP. Bis A or octylphenols had no effect on 125I-hCG binding to Leydig cell LH-receptors. Thus, these environmental chemicals appear to inhibit cAMP formation and steroidogenesis in mLTC-1 Leydig tumor cells by preventing the coupling between LH receptor and the adenylate cyclase. Since, estradiol did not inhibit hCG-stimulated cAMP production, the effects of bis A and octylphenols may not be estrogen related. This emphasizes the complexity of endocrine disruption: chemicals show multiple endocrine activities that may disturb several organs in distinct ways.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/4-octylphenol,
http://linkedlifedata.com/resource/pubmed/chemical/4-tert-octylphenol,
http://linkedlifedata.com/resource/pubmed/chemical/8-Bromo Cyclic Adenosine...,
http://linkedlifedata.com/resource/pubmed/chemical/Cholera Toxin,
http://linkedlifedata.com/resource/pubmed/chemical/Chorionic Gonadotropin,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic AMP,
http://linkedlifedata.com/resource/pubmed/chemical/Environmental Pollutants,
http://linkedlifedata.com/resource/pubmed/chemical/Estrogens, Non-Steroidal,
http://linkedlifedata.com/resource/pubmed/chemical/Forskolin,
http://linkedlifedata.com/resource/pubmed/chemical/Phenols,
http://linkedlifedata.com/resource/pubmed/chemical/Progesterone,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, LH,
http://linkedlifedata.com/resource/pubmed/chemical/Steroids,
http://linkedlifedata.com/resource/pubmed/chemical/bisphenol A
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0041-008X
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pubmed:author | |
pubmed:copyrightInfo |
Copyright 1999 Academic Press.
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pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
157
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
166-73
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pubmed:dateRevised |
2003-11-14
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pubmed:meshHeading |
pubmed-meshheading:10373400-8-Bromo Cyclic Adenosine Monophosphate,
pubmed-meshheading:10373400-Animals,
pubmed-meshheading:10373400-Cholera Toxin,
pubmed-meshheading:10373400-Chorionic Gonadotropin,
pubmed-meshheading:10373400-Cyclic AMP,
pubmed-meshheading:10373400-Environmental Pollutants,
pubmed-meshheading:10373400-Estrogens, Non-Steroidal,
pubmed-meshheading:10373400-Forskolin,
pubmed-meshheading:10373400-Leydig Cell Tumor,
pubmed-meshheading:10373400-Leydig Cells,
pubmed-meshheading:10373400-Male,
pubmed-meshheading:10373400-Mice,
pubmed-meshheading:10373400-Phenols,
pubmed-meshheading:10373400-Progesterone,
pubmed-meshheading:10373400-Receptors, LH,
pubmed-meshheading:10373400-Steroids,
pubmed-meshheading:10373400-Tumor Cells, Cultured
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pubmed:year |
1999
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pubmed:articleTitle |
Inhibition of hCG-stimulated steroidogenesis in cultured mouse Leydig tumor cells by bisphenol A and octylphenols.
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pubmed:affiliation |
Department of Physiology, University of Turku, Turku, FIN-20520, Finland.
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pubmed:publicationType |
Journal Article
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