کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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2594557 | 1132272 | 2009 | 9 صفحه PDF | دانلود رایگان |
Exposure to antiandrogens during the critical developmental window (i.e. sexual differentiation) can permanently demasculinize the male phenotype. Here we have investigated the effects of developmental exposure to di-isononylphthalate (DINP) (250 and 750 mg/kg) and 1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene (p,p′-DDE) (50 and 100 mg/kg) on 19.5-day-old fetal Sprague–Dawley rat testicular and adrenal steroidogenesis. Maternal exposure to DINP or p,p′-DDE on embryonic days (EDs) 13.5–17.5 did not down-regulate the activity of steroidogenesis in ED 19.5 male rat fetus. Protein expression levels of testicular and adrenal StAR, P450scc, 3β-HSD and androgen receptor (AR) did not show any changes. However, p,p′-DDE caused clear abnormalities in the ultrastructure of steroidogenic cells in ED 19.5 rat testis and adrenal. These structural alterations can disturb the development and function of fetal testis and adrenal that may become evident later in life.
Journal: Reproductive Toxicology - Volume 28, Issue 1, July 2009, Pages 66–74