Record Display for the EPA National Library Catalog

RECORD NUMBER: 25 OF 97

OLS Field Name OLS Field Data
Main Title Effect of Cadmium and Other Metal Cations on In vitro Leydig Cell Testosterone Production.
Author Laskey, J. W. ; Phelps., P. V. ;
CORP Author Health Effects Research Lab., Research Triangle Park, NC. Reproductive Toxicology Branch.
Publisher c1991
Year Published 1991
Report Number EPA/600/J-91/092;
Stock Number PB91-200261
Additional Subjects Cadmiums ; Toxicology ; Leydig cells ; Testosterone ; Cations ; Biosynthesis ; In vivo analysis ; Chorionic gonadotropins ; Radioimmunoassay ; Dose-response relationships ; In vitro analysis ; Cyclic 3',5'-adenosine monophosphate ; Rats ; Cultured cells ; Reprints ;
Holdings
Library Call Number Additional Info Location Last
Modified
Checkout
Status
NTIS  PB91-200261 Most EPA libraries have a fiche copy filed under the call number shown. Check with individual libraries about paper copy. 09/04/1991
Collation 14p
Abstract
In vivo assessment of toxicant action on Leydig cell function is subject to homeostatic mechanisms which make it difficult to determine whether any changes seen in serum testosterone (T) concentration are due to extragonadal endocrine alterations or to a direct effect on the Leydig cell. Studies used a testicular cell culture technique to evaluate Leydig cell testosterone biosynthesis in the presence of several metal cations. To determine the site of toxic action, the Leydig cells were stimulated to produce testosterone by using human chorionic gonadotrophin (hCG), dibutyl cyclic adenosine monophosphate (db cAMP) or several substrates required for the biosynthesis of testosterone. Ca(2+), Cr(3+), Fe(3+), Mg(2+), Na(1+) or Pb(2+) had no effect on stimulated testosterone. Dose response depression in both hCG and db-cAMP stimulated testosterone production were seen with Cd(2+), Co(2+), Cu(2+), Hg(2+), Ni(2+), and Zn(2+) treatment. Surprisingly several of the metal cations which caused a depression in hCG and db cAMP stimulated testosterone production caused significant increases in HCHOL and PREG stimulated testosterone production over untreated and similarly stimulated cultures.