Adamsson A, Salonen V, Paranko J, Toppari J
Department of Physiology, University of Turku, 20520 Turku, Finland.
Reprod Toxicol. 2009 Jul;28(1):66-74. doi: 10.1016/j.reprotox.2009.03.002. Epub 2009 Mar 20.
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 100mg/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, 3beta-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.
在关键发育窗口（即性分化期）接触抗雄激素会使雄性表型永久去雄性化。在此，我们研究了发育过程中接触邻苯二甲酸二异壬酯（DINP）（250和750毫克/千克）以及1,1 - 二氯 - 2,2 - 双（对氯苯基）乙烯（p,p'-DDE）（50和100毫克/千克）对19.5日龄胎儿斯普拉格 - 道利大鼠睾丸和肾上腺类固醇生成的影响。在胚胎期（EDs）13.5 - 17.5时母体接触DINP或p,p'-DDE，并未下调19.5日龄雄性大鼠胎儿的类固醇生成活性。睾丸和肾上腺类固醇生成急性调节蛋白（StAR）、细胞色素P450侧链裂解酶（P450scc）、3β - 羟基类固醇脱氢酶（3β - HSD）和雄激素受体（AR）的蛋白表达水平未显示任何变化。然而，p,p'-DDE导致19.5日龄大鼠睾丸和肾上腺中类固醇生成细胞的超微结构出现明显异常。这些结构改变可能会干扰胎儿睾丸和肾上腺的发育及功能，这在以后的生命中可能会变得明显。
