Linked Life Data

12606426

Source:http://linkedlifedata.com/resource/pubmed/id/12606426

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2003-4-22
pubmed:abstractText
The pubertal initiation of spermatogenesis is reliant on androgens, and during this time, 5alpha-reduced androgens such as dihydrotestosterone (DHT) are the predominant androgens in the testis. Two 5alpha-reductase (5alphaR) isoenzymes (5alphaR1 and 5alphaR2) have been identified, which catalyze the conversion of testosterone to the more potent androgen DHT. The present study aimed to investigate the developmental pattern of 5alphaR isoenzymes and their relationship to the production of 5alpha-reduced androgens in the postnatal rat testis. Both 5alphaR1 and 5alphaR2 isoenzyme mRNAs were measured by real-time polymerase chain reaction, isoenzyme activity levels by specific assays, and testicular androgens by radioimmunoassay after high-performance liquid chromatographic separation. Both 5alphaR1 and 5alphaR2 mRNAs and activity levels were low in the 10-day-old (prepubertal) testis, peaked between Days 20 and 40 during puberty, and then declined to low levels at 60-160 days of age. The developmental pattern of both 5alphaR isoenzyme activity levels was mirrored by the testicular production of 5alpha-reduced metabolites. Although 5alphaR1 was greater than 5alphaR2 at all ages, it is likely, given the substrate preferences of the two, that both isoenzymes contribute to the pubertal peak of 5alpha-reduced androgen biosynthesis. The peak in 5alphaR isoenzymes and 5alpha-reduced metabolite production coincided with the first wave of spermatogenesis in the rat, suggesting a role for 5alpha-reduced metabolites in the initiation of spermatogenesis. This was explored by acute administration of a 5alphaR inhibitor (L685,273) to immature rats. The L685,273 markedly suppressed testicular 5alphaR activity during puberty by 75%-86%. However, a marked increase was observed in testicular testosterone levels (in the absence of changes in LH), and no decrease was observed in the absolute levels of 5alpha-reduced metabolites. Therefore, whether the formation of DHT in the presence of low testosterone levels in the pubertal testis is required for the initiation of spermatogenesis cannot be tested using 5alphaR inhibitors. We conclude that both 5alphaR1 and 5alphaR2 isoenzymes are involved in the peak of 5alpha-reduced androgen biosynthesis in the testis during the pubertal initiation of spermatogenesis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0006-3363
pubmed:author
pubmed:issnType
Print
pubmed:volume
68
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1711-8
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:12606426-3-Oxo-5-alpha-Steroid 4-Dehydrogenase, pubmed-meshheading:12606426-5-alpha Reductase Inhibitors, pubmed-meshheading:12606426-Androgens, pubmed-meshheading:12606426-Animals, pubmed-meshheading:12606426-Animals, Newborn, pubmed-meshheading:12606426-Enzyme Inhibitors, pubmed-meshheading:12606426-Follicle Stimulating Hormone, pubmed-meshheading:12606426-Gonadotropins, pubmed-meshheading:12606426-Indicators and Reagents, pubmed-meshheading:12606426-Isoenzymes, pubmed-meshheading:12606426-Luteinizing Hormone, pubmed-meshheading:12606426-Male, pubmed-meshheading:12606426-Organ Size, pubmed-meshheading:12606426-Pregnenediones, pubmed-meshheading:12606426-Prostate, pubmed-meshheading:12606426-Rats, pubmed-meshheading:12606426-Rats, Sprague-Dawley, pubmed-meshheading:12606426-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:12606426-Spermatogenesis, pubmed-meshheading:12606426-Testis
pubmed:year
2003
pubmed:articleTitle
5alpha-reductase isoenzymes 1 and 2 in the rat testis during postnatal development.
pubmed:affiliation
Prince Henry's Institute of Medical Research, Clayton, Victoria 3168, Australia.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't