Abstract:
:We previously described significant differences in maximal testosterone production by Leydig cells from the following strains of inbred mice: C57BL/10J, C57BL/6J, DBA/2J, and C3H/HeJ. To evaluate whether these differences in maximal testosterone production related to the activities of the steroidogenic enzymes of the smooth endoplasmic reticulum of Leydig cells from these strains, the activities of 3 beta-hydroxysteroid dehydrogenase-isomerase, 17 alpha-hydroxylase, C17-20 lyase, and 17-ketosteroid reductase were measured in homogenates of purified Leydig cells using 3H-labeled substrates and measuring the amounts of 3H products formed. Maximal and basal testosterone production were determined by incubating aliquots of Leydig cells for 2 h in the presence or absence of 30 pM hCG. Maximal testosterone production by Leydig cells from C57BL/10J and C57BL/6J mice was significantly greater than that by Leydig cells from DBA/2J and C3H/HeJ mice. No difference in basal testosterone production was observed among the strains. Among the four enzymes studied, only 3 beta-hydroxysteroid dehydrogenase-isomerase activity was significantly correlated with hCG-stimulated testosterone production by Leydig cells from the four strains of mice. In addition, when equivalent numbers of Leydig cells from each strain were incubated with an equal concentration of [3H]pregnenolone, a similar difference in [3H] testosterone production was observed among the four strains, as was seen with hCG-stimulation. Leydig cells from C57BL/10 and C57BL/6J mice left less [3H]pregnenolone unmetabolized and produced higher amounts of [3H]testosterone than Leydig cells from DBA/2J and C3H/HeJ mice. There was a significant negative correlation between the amount of pregnenolone unmetabolized and the amount of testosterone produced. These data suggest that 3 beta-hydroxysteroid dehydrogenase-isomerase may be important in determining the differences in hCG-stimulated testosterone production by Leydig cells from the four strains of mice.
journal_name
Endocrinologyjournal_title
Endocrinologyauthors
Stalvey JR,Payne AHdoi
10.1210/endo-115-4-1500subject
Has Abstractpub_date
1984-10-01 00:00:00pages
1500-5issue
4eissn
0013-7227issn
1945-7170journal_volume
115pub_type
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