Testosterone Decreases 3 Beta-hydroxysteroid Dehydrogenase-isomerase Messenger Ribonucleic Acid In Cultured Mouse Leydig Cells By A Strain-specific Mechanism
17-alpha-hydroxylase/c17-20 lyase; adult-rats; androgen; denovo synthesis; Endocrinology & Metabolism; expression; human chorionic-gonadotropin; inbred mice; luteinizing-hormone; receptor; rna; side-chain cleavage; steroidogenesis; testicular cells; testis
We previously reported a strain-related difference in basal 3 beta-hydroxysteroid dehydrogenase-isomerase (3 beta HSD) activity in response to testosterone in cultured Leydig cells. The data suggested that the response to testosterone was androgen receptor mediated and that testosterone was acting via a irans-acting factor distal to the androgen receptor to regulate Leydig cell basal 3 beta HSD activity. This study was designed to determine whether the previous reported strain-related difference in basal 3 beta HSD activity in response to testosterone was due to a difference at the 3 beta HSD protein and/or at the mRNA level, In C57BL/6J Leydig cells, 2.0 mu M testosterone significantly decreased basal 3 beta HSD immunoreactive mass by day 6 in culture. Treatment with 2.0 mu M testosterone and 2.0 mu M hydroxyflutamide, an androgen receptor antagonist, negated the inhibitory effect of testosterone on C57BL/6J 3 beta HSD immunoreactive mass, Treatment with 2.0 mu M testosterone also significantly decreased 3 beta HSD mRNA content in C57BL/6J Leydig cells, which was detectable on day 3 in culture, In contrast to Leydig cells from C57BL/6J mice, Leydig cells from C3H/HeJ mice were not susceptible to the inhibitory effect of testosterone on 3 beta HSD. Treatment with 2.0 mu M testosterone had no detectable effect on C3H/HeJ 3 beta HSD immunoreactive mass or mRNA content at any time point in culture. These data indicate that the testosterone-induced loss of basal 3 beta HSD activity in C57BL/6J Leydig cells can he accounted for by the lass of 3 beta HSD immunoreactive mass, which is preceded by the loss of 3 beta HSD mRNA, and that the strain-related difference in the regulation of 3 beta HSD is present at all three levels. Thus, the putative trans-acting factor involved in the mechanism whereby testosterone decreases basal 3 beta HSD is likely to regulate the amount of 3 beta HSD mRNA.
Heggland S J; Signs S A; Stalvey J R D
Journal of Andrology
1997
1997-11
Journal Article or Conference Abstract Publication
n/a
The Ability Of The Quadruple Test To Predict Adverse Perinatal Outcomes In A High-risk Obstetric Population
alpha-fetoprotein; association; birth; down-syndrome; Environmental & Occupational Health; human chorionic-gonadotropin; intrauterine growth restriction; markers; maternal; preeclampsia; pregnancy; Public; serum inhibin
`Objective To determine the ability of the quadruple Down's syndrome screening test (quad screen) to predict other adverse perinatal outcomes (APO) in a high-risk obstetric population. Setting A tertiary medical centre in West Virginia. Methods We retrospectively reviewed 342 obstetric patients with quad screen data from a single clinic. The quad screen included maternal serum levels of alphafetoprotein (AFP), human chorionic gonadotrophin (hCG), uncongjugated oestriol (uE(3)) and inhibin A. The risk of APO was compared between patients with at least one abnormal marker versus no abnormal markers and >= 2 abnormal markers versus <2 abnormal markers. Abnormal markers were determined by cut-off values produced by Receiver Operator Characteristic (ROC) curves and the FASTER trial. Unadjusted and adjusted effects were estimated using logistic regression analysis. Results The risk of having an APO increased significantly for patients with abnormal markers by about three-fold using ROC and two-fold using FASTER trial thresholds. Conclusions The quad screen shows value in predicting risk of APO in high-risk patients.
Lao M R; Calhoun B C; Bracero L A; Wang Y; Seybold D J; Brace M; Hatjis C G
Journal of Medical Screening
2009
2009
Journal Article or Conference Abstract Publication
<a href="http://doi.org/10.1258/jms.2009.009017" target="_blank" rel="noreferrer noopener">10.1258/jms.2009.009017</a>