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Department of Physiology and Biophysics (K.H.H., T.D., S.G., B.K.S., M.R., H.B.B., D.B.H.), University of Illinois at Chicago, Chicago, Illinois 60612-7342; and Department of Urology (T.D.), University Hospital of the Justus-Liebig-University, 35392 Giessen, Germany
Address all correspondence and requests for reprints to: Dale B. Hales, Department of Physiology and Biophysics, University of Illinois at Chicago, 835 South Wolcott Avenue, Chicago, Illinois 60612-7342. E-mail: dbhale{at}uic.edu
Immune activation results in the activation of adrenal steroidogenesis
and inhibition of gonadal steroidogenesis. Previous studies indicated
that these effects were caused primarily by activation and suppression
of the secretion of ACTH and LH, respectively. However, other evidence
indicated a direct effect of the immune system on the gonads. In this
study, serum testosterone, quantitated by RIA after
lipopolysaccharide injection, showed a significant decrease
within 2 h. Parallel measurement of serum LH showed no change.
There were no differences in LH receptor or cAMP produced in Leydig
cells between vehicle- and lipopolysaccharide-injected mice. The 30-kDa
form of the steroidogenic acute regulatory (StAR) protein was
quantitated, by Western blot, in Leydig cells and was found to decrease
in a time-dependent manner. No change in StAR protein messenger RNA
(mRNA) was detected by Northern analysis during this time, nor were any
changes found in the levels of mRNA for the steroidogenic enzymes
P450scc, 3ß-hydroxysteroid dehydrogenase
4-
5-isomerase, or P450c17. In the
adrenal, StAR protein was increased, as was StAR protein mRNA. No
changes were observed in the levels of mRNA for P450scc,
3ß-hydroxysteroid dehydrogenase
4-
5-isomerase, or P450c21. Thus, although
the mechanisms of regulation differ, changes in the levels of StAR
protein are a sensitive indicator of the steroidogenic capacity of
these two tissues.
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