pubmed-article:2251676 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:2251676 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
pubmed-article:2251676 | lifeskim:mentions | umls-concept:C0205070 | lld:lifeskim |
pubmed-article:2251676 | lifeskim:mentions | umls-concept:C0405581 | lld:lifeskim |
pubmed-article:2251676 | lifeskim:mentions | umls-concept:C0373704 | lld:lifeskim |
pubmed-article:2251676 | lifeskim:mentions | umls-concept:C0021467 | lld:lifeskim |
pubmed-article:2251676 | lifeskim:mentions | umls-concept:C0332152 | lld:lifeskim |
pubmed-article:2251676 | lifeskim:mentions | umls-concept:C0597513 | lld:lifeskim |
pubmed-article:2251676 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
pubmed-article:2251676 | lifeskim:mentions | umls-concept:C1562566 | lld:lifeskim |
pubmed-article:2251676 | lifeskim:mentions | umls-concept:C1522492 | lld:lifeskim |
pubmed-article:2251676 | lifeskim:mentions | umls-concept:C1709305 | lld:lifeskim |
pubmed-article:2251676 | lifeskim:mentions | umls-concept:C0332120 | lld:lifeskim |
pubmed-article:2251676 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:2251676 | pubmed:dateCreated | 1991-1-17 | lld:pubmed |
pubmed-article:2251676 | pubmed:abstractText | The mechanism by which 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) treatment decreases testosterone (T) secretion without significantly altering plasma luteinizing hormone (LH) concentrations was investigated. Testes from sexually mature Sprague-Dawley rats dosed 7 days earlier with 100 micrograms TCDD/kg secreted 30-75% less T than did testes from control rats when perfused in vitro with the LH analog human chorionic gonadotropin (hCG). This decrease confirms that testicular responsiveness to LH, the hormone which regulates T secretion in vivo, is impaired by TCDD treatment. Because TCDD also reduced intratesticular T content, the decrease in T secretion is due to an inhibition of T synthesis rather than to a failure of the secretion process. These effects of TCDD are not secondary to undernutrition, because perfused testes from feed-restricted control rats were fully hCG responsive. TCDD treatment neither increased the hCG-stimulated secretion of any T precursor nor significantly decreased the efficiency with which testes converted the pregnenolone (PREG) they synthesized into T (PREG is the initial steroidogenic intermediate). In addition, TCDD did not inhibit T secretion when steroidogenesis was supported by exogenous PREG at approximately the in vivo rate. We conclude that TCDD does not inhibit the conversion of PREG to T. The inhibition of T biosynthesis must instead result from an inhibition of PREG formation. The finding that TCDD treatment substantially decreased the rate at which hCG-perfused testes secreted PREG and its metabolites (a decrease seen across all hCG concentrations) confirms this conclusion. This inhibition of LH/hCG-stimulated PREG formation by TCDD must be due to a reduction in the activity of the enzyme which converts cholesterol to PREG (cytochrome P450scc), and/or an impairment in the multistep process responsible for mobilizing cholesterol to this enzyme. | lld:pubmed |
pubmed-article:2251676 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2251676 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2251676 | pubmed:language | eng | lld:pubmed |
pubmed-article:2251676 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2251676 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:2251676 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2251676 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2251676 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2251676 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2251676 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2251676 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:2251676 | pubmed:month | Oct | lld:pubmed |
pubmed-article:2251676 | pubmed:issn | 0041-008X | lld:pubmed |
pubmed-article:2251676 | pubmed:author | pubmed-author:PetersonR ERE | lld:pubmed |
pubmed-article:2251676 | pubmed:author | pubmed-author:MooreR WRW | lld:pubmed |
pubmed-article:2251676 | pubmed:author | pubmed-author:KleemanJ MJM | lld:pubmed |
pubmed-article:2251676 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:2251676 | pubmed:volume | 106 | lld:pubmed |
pubmed-article:2251676 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:2251676 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:2251676 | pubmed:pagination | 112-25 | lld:pubmed |
pubmed-article:2251676 | pubmed:dateRevised | 2007-11-15 | lld:pubmed |
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pubmed-article:2251676 | pubmed:year | 1990 | lld:pubmed |
pubmed-article:2251676 | pubmed:articleTitle | Inhibition of testicular steroidogenesis in 2,3,7,8-tetrachlorodibenzo-p-dioxin-treated rats: evidence that the key lesion occurs prior to or during pregnenolone formation. | lld:pubmed |
pubmed-article:2251676 | pubmed:affiliation | Environmental Toxicology Center, University of Wisconsin, Madison 53706. | lld:pubmed |
pubmed-article:2251676 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:2251676 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:2251676 | lld:pubmed |