Document Detail


In vitro effects of estradiol, diethylstilbestrol and tamoxifen on testosterone production by purified pig Leydig cells.
MedLine Citation:
PMID:  1667095     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The direct effects of estradiol-17 beta (E2), diethylstilbestrol (DES) and tamoxifen on testicular testosterone production by purified immature pig Leydig cells in vitro were studied. Leydig cells were obtained from 3-4 weeks old piglet testes by enzymatical dispersion followed by discontinuous Percoll gradient centrifugation. Leydig cells were treated with E2, DES, and tamoxifen in the absence or presence of LH after 12 h of incubation. Media were collected 48 h later for testosterone and cAMP measurement. E2 did not affect basal testosterone production. When Leydig cells were incubated with increasing concentrations (0.001-10.0 micrograms/ml) of E2, DES, or tamoxifen for 48 h, LH-stimulated testosterone production was reduced. The degree of this reduction was dependent on E2, DES, and tamoxifen, and a concentration of E2 and DES and tamoxifen higher than 100 ng/ml and 10 ng/ml was needed, respectively. DES and tamoxifen also reduced LH-stimulated cAMP formation. When equal concentrations of DES and tamoxifen were added concomitantly to Leydig cells, the inhibition was additive, indicating that tamoxifen does not prevent the inhibitory effects of DES. Forskolin, an activator of adenylate cyclase, stimulated testosterone production to an extent comparable to that attained with LH, and DES and tamoxifen reduced forskolin-stimulated testosterone production. DES and tamoxifen suppressed the conversion of exogenous pregnenolone and progesterone to testosterone, but did not affect the conversion of 17 alpha-hydroxyprogesterone to testosterone, suggesting a specific inhibition of 17 alpha-hydroxylase. These results suggest that E2, DES, and tamoxifen directly inhibit immature pig Leydig cell steroidogenesis, at least in part via an inhibition of cAMP formation and a decrease in the activity of 17 alpha-hydroxylase.
Authors:
P S Li
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Chinese journal of physiology     Volume:  34     ISSN:  0304-4920     ISO Abbreviation:  Chin J Physiol     Publication Date:  1991  
Date Detail:
Created Date:  1992-05-26     Completed Date:  1992-05-26     Revised Date:  2009-08-12    
Medline Journal Info:
Nlm Unique ID:  7804502     Medline TA:  Chin J Physiol     Country:  TAIWAN    
Other Details:
Languages:  eng     Pagination:  287-301     Citation Subset:  IM    
Affiliation:
Department of Physiology, College of Medicine, National Cheng Kung University, Tainan, Taiwan, R.O.C.
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MeSH Terms
Descriptor/Qualifier:
17-alpha-Hydroxyprogesterone
Animals
Cyclic AMP / biosynthesis
Diethylstilbestrol / pharmacology*
Estradiol / pharmacology*
Forskolin / pharmacology
Hydroxyprogesterones / pharmacology
Leydig Cells / drug effects,  metabolism*
Luteinizing Hormone / pharmacology
Male
Pregnenolone / metabolism
Progesterone / metabolism
Radioimmunoassay
Swine
Tamoxifen / pharmacology*
Testosterone / biosynthesis*
Chemical
Reg. No./Substance:
0/Hydroxyprogesterones; 10540-29-1/Tamoxifen; 145-13-1/Pregnenolone; 50-28-2/Estradiol; 56-53-1/Diethylstilbestrol; 57-83-0/Progesterone; 58-22-0/Testosterone; 60-92-4/Cyclic AMP; 66428-89-5/Forskolin; 68-96-2/17-alpha-Hydroxyprogesterone; 9002-67-9/Luteinizing Hormone
Comments/Corrections
Erratum In:
Chin J Physiol 1991;34(4):464

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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