Effects of inducible nitric oxide synthase (iNOS) deficiency in mice on Sertoli cell proliferation and perinatal testis development

S A Auharek, N L M Lara, G F Avelar, R M Sharpe, L R França

Research output: Contribution to journalArticlepeer-review

Abstract

Nitric oxide (NO) plays crucial roles in several physiological and pathological conditions. The iNOS isoform produces high levels of NO independent of intracellular calcium and, in the testis, which is expressed in Sertoli (SC), Leydig (LC) and germ cells. The testicular roles of NO are unclear, but it can inhibit LC testosterone production. Our aim was to evaluate the effects of iNOS deficiency on testis development in mice from late fetal life through early puberty. Therefore, testes from wild type (C57BCL/6) and iNOS(-/-) mice (B6.129P2- Nos2(tm1Lau) /J) were sampled at various ages between e18.5 and Pnd20 and evaluated by histological and stereological analyses; proliferating cells were labelled with (3) H-thymidine. At all ages, testis weight and anogenital index, a measure of fetal androgen exposure, were greater in iNOS-deficient mice than in wild type mice. At all ages after birth, iNOS-deficient mice exhibited increased (p 
Original languageEnglish
JournalInternational Journal of Andrology
DOIs
Publication statusPublished - 2012

Fingerprint Dive into the research topics of 'Effects of inducible nitric oxide synthase (iNOS) deficiency in mice on Sertoli cell proliferation and perinatal testis development'. Together they form a unique fingerprint.

Cite this