间质细胞
内分泌学
内科学
GNRHR公司
胆固醇侧链裂解酶
胎儿
邻苯二甲酸盐
内卷(密宗)
睾酮(贴片)
邻苯二甲酸二丁酯
生物
玉米油
医学
化学
怀孕
促黄体激素
新陈代谢
促性腺激素释放激素
激素
意识
遗传学
有机化学
细胞色素P450
神经科学
作者
Xiaomin Chen,Linxi Li,Huitao Li,Hongguo Guan,Yaoyao Dong,Xiaoheng Li,Qiufan Wang,Qingquan Lian,Guoxin Hu,Ren‐Shan Ge
出处
期刊:Toxicology
[Elsevier]
日期:2017-07-01
卷期号:386: 19-27
被引量:25
标识
DOI:10.1016/j.tox.2017.05.004
摘要
Fetal exposure to di-n-butyl phthalate (DBP) causes the adult disease such as lower testosterone production and infertility. However, the mechanism is still unknown. The objective of the present study is to determine how DBP affects the involution of fetal Leydig cells during the neonatal period and how this event causes the delayed development of the adult Leydig cells during puberty. The pregnant Sprague Dawley dams were randomly divided into 3 groups and were gavaged with 0 (corn oil, the vehicle control), 100 or 500mg/kg DBP from gestational day 12 (G12) to G21. The blood and testes were collected from male pups on postnatal day 4 (P4), P7, P14, P21, P28, and P56. Serum testosterone concentrations were assessed and the mRNA levels of Leydig cell- or gonadotroph cell-specific genes were measured. Prenatal exposure to DBP caused the aggregation of fetal Leydig cells, which slowly disappeared when compared to the control. This effect was associated with the reduction of testicular testosterone secretion and down-regulation of the mRNA levels of Leydig cell biomarkers including Scarb1, Star, Cyp11a1, Hsd3b1, Hsd11b1, and Hsd17b3 as well as the gonadotroph biomarkers including Lhb and Gnrhr. In conclusion, we demonstrated that the increased aggregation of fetal Leydig cells by DBP delayed fetal Leydig cell involution, thus leading to the disrupted development of the adult Leydig cells.
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