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5-alpha-reductase and the development of the human prostate.
Indian J Urol ; 24(3): 309-12, 2008 Jul.
Article em En | MEDLINE | ID: mdl-19468459
During the 10(th) week of gestation human prostate development is about to start. Androgens are the crucial factors to stimulate the initial interactions between the epithelium and mesenchyme. One of the key events in androgen metabolism is the transformation of circulating testosterone to 5alpha-dihydrotestosterone (DHT) by tissue-linked 5alpha-reductase. Both, the formation of a male phenotype and the androgen-mediated growth of the prostate are mediated by DHT. To date the function of 5alpha-reductase 1 (5alphaR1) still remains unclear whereas 5alpha-reductase 2 (5alphaR2) is supposed to be the predominant isoenzyme in human accessory sex tissue. Only little data are available on the detection, distribution, and effects of both isoenzymes during fetal life and infancy. Recently, immunohistochemical investigations of serial sections from fetuses and infants using specific antibodies directed against 5alphaR1 and 5alphaR2 seem to shed light on that issue. Moreover, the detection of downstream products of androgen synthesis using RT-PCR analyses for 17-beta hydroxysteroid dehydrogenase Type 2 (17 betaHSD 2), 17 betaHSD Type 3 and 17 betaHSD Type 7 adds to discovering the molecular biological background. New studies confirm that both isoenzymes are present throughout fetal development. On the transcriptional level RT-PCR for 5alphaR1 and 5alphaR2 certifies these findings. 17 betaHSD 2, 3 and 7 representing the most relevant enzymatic downstream products of cellular androgen synthesis were revealed by RT-PCR as well. Current studies discovered the expression and distribution of both 5alpha-reductase isoenzymes as well as the potential contribution of 5alphaR1 during fetal human prostate development.
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Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2008 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2008 Tipo de documento: Article