In utero exposure to diisononyl phthalate caused testicular dysgenesis of rat fetal testis

Diisononyl phthalate (DINP) is a synthetic material that has been widely used as a substitute for other plasticizers prohibited due to reproductive toxicity in consumer products. Some phthalates have been associated with testicular dysgenesis syndrome in male fetus when female pregnant dams were exp...

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Bibliographic Details
Published in:Toxicology letters 2015-01, Vol.232 (2), p.466-474
Main Authors: Li, Linxi, Bu, Tiao, Su, Huina, Chen, Zhichuan, Liang, Yuyuan, Zhang, Gaolong, Zhu, Danyan, Shan, Yuanyuan, Xu, Renai, Hu, Yuanyuan, Li, Junwei, Hu, Guoxin, Lian, Qingquan, Ge, Ren-Shan
Format: Article
Language:English
Subjects:
Agglomeration
Exposure
Females
Gene expression
Genes
Phthalates
Proteins
Testosterone
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Summary:Diisononyl phthalate (DINP) is a synthetic material that has been widely used as a substitute for other plasticizers prohibited due to reproductive toxicity in consumer products. Some phthalates have been associated with testicular dysgenesis syndrome in male fetus when female pregnant dams were exposed to them. The present study investigated effects of DINP on fetal Leydig cell function and testis development. Female pregnant Sprague Dawley rats received control vehicle (corn oil) or DINP (10, 100, 500, and 1000mg/kg) by oral gavage from gestational day (GD) 12 to 21. At GD 21.5, testicular testosterone production, fetal Leydig cell numbers and distribution, testicular gene and protein expression levels were examined. DINP showed dose-dependent increase of fetal Leydig cell aggregation with the low observed adverse-effect level (LOAEL) of 10mg/kg and multinucleated gonocyte with LOAEL of 100mg/kg. At 10mg/kg, DINP also significantly increased fetal Leydig cell size, but inhibited insulin-like 3 and 3 beta -hydroxysteroid dehydrogenase gene expression and protein levels. DINP inhibited testicular testosterone levels at 1000mg/kg. The results indicate that in utero exposure to DINP affects the expression levels of some fetal Leydig cell steroidogenic genes, gonocyte multinucleation and Leydig cell aggregation.
ISSN:0378-4274
DOI:10.1016/j.toxlet.2014.11.024