Absence of correlation between in situ expression of cytochrome P450 17 alpha hydroxylase/lyase and 3 beta-hydroxysteroid dehydrogenase/(Delta 5-4) isomerase messenger ribonucleic acids and steroidogenesis during pubertal development in the rat testis

Changes in expression of Leydig cell 3 beta-hydroxysteroid dehydrogenase (3 beta HSD) and 17 alpha-hydroxylase/C17-20 lyase (P450(17 alpha)) messenger RNA (mRNA) during pubertal development have not been well characterized in the rat. In the present study, expression of 3 beta HSD and P450(17 alpha) were determined in frozen sections of testes of immature (days 21 and 28), pubertal (days 45 and 60) and adult (day 90) rats by in situ hybridization using digoxigenin-labeled riboprobes and quantified densitometrically. Mea sures of steroidogenesis in this study, 3 beta HSD and P450(17 alpha) enzym e activities per testis and plasma testosterone concentration, increased du ring pubertal development, peaking at 45-60 days of age. Expression of 3 be ta HSD protein, a marker for Leydig cell function, was abundantly immunoloc alized to the interstitial compartment of the testis. Quantified densitomet rically, the amount of 3 beta HSD protein did not vary significantly during pubertal development. Transcripts of 3 beta HSD and P450(17 alpha) were ex pressed abundantly by clusters of immature Leydig cells in immature animals . However, in contrast to measures of steroidogenesis during pubertal devel opment, mRNA of 3 beta HSD and P450(17 alpha) decreased to undetectable lev els at the age of 45 and 60 days, respectively. The decline in mRNA of 3 be ta HSD and P450(17 alpha) was confirmed by Northern analysis. Expression of 3 beta HSD and P450(17 alpha) transcripts rebounded in the adult at 90 day s and were comparable to levels of expression observed in immature animals. These results show that during pubertal development the steady-state accum ulation of mRNA of 3 beta HSD and P450(17 alpha) are not correlated with ac cumulation of 3 beta HSD protein, enzyme activities of 3 beta HSD and P450( 17 alpha), or testosterone secretion. Possible explanations of the depletio n of transcripts during pubertal development include: specific inhibition o f transcription, increased mRNA instability, or high translational activity . (C) 2000 Elsevier Science Ltd. All rights reserved.