In:
Birth Defects Research Part B: Developmental and Reproductive Toxicology, Wiley, Vol. 95, No. 4 ( 2012-08), p. 318-325
Kurzfassung:
Previous research from our laboratory has determined the transcript profiles for developing fetal rat female and male reproductive tracts following transplacental exposure to estrogens. Prenatal exposure to bisphenol A ( BPA ) or 17‐α‐ethynyl estradiol ( EE ) significantly affects steroidogenic acute regulatory ( S t AR ) protein transcript levels in the developing male rat reproductive tract. The purpose of this study was to establish the intratesticular distribution and temporal expression pattern of S t AR , a key gene involved in steroidogenesis. Beginning on gestation day ( GD ) 11, pregnant S prague‐ D awley rats were exposed daily to 10μg/kg/day EE and fetal testes were harvested at GD 16, 18, or 20. Quantitative reverse transcriptase PCR ( QRT ‐ PCR ) demonstrated no significant difference in S t AR transcript levels present at GD 16. However, at GD 18, S t AR transcripts were significantly decreased following exposure. Immunohistochemistry demonstrated similar S t AR protein levels in interstitial region of GD 16 testes and an obvious decrease in S t AR protein levels in the interstitial region of GD 18 testes. Moreover, starting at GD 11 additional dams were dosed with 0.001 or 0.1 μg/kg/day EE or 0.02, 0.5, 400 mg/kg/day BPA via subcutaneous injections. QRT ‐ PCR validated previous microarray dose‐related decreases in S t AR transcripts at GD 20, whereas immunohistochemistry results demonstrated decreases in S t AR protein levels in the interstitial region at the highest EE and BPA doses only. Neither EE nor BPA exposure caused morphological changes in the developing seminiferous cords, S ertoli cells, gonocytes, or the interstitial region or L eydig cells at GD 16–20. High levels of estrogens decrease S t AR expression in the fetal rat testis during late gestation.
Materialart:
Online-Ressource
ISSN:
1542-9733
,
1542-9741
DOI:
10.1002/bdrb.2012.95.issue-4
Sprache:
Englisch
Verlag:
Wiley
Publikationsdatum:
2012
ZDB Id:
2108625-4