Carcinogenesis, Teratogenesis & Mutagenesis

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The effects of di(2-ethylhexyl ) phthalate on hormonal- related gene expression levels in male rats'

QIN Xiao-yun1,2,TAN Qin1,2,XU Xin-yun1,*,WU De-sheng1,HUANG Hai-yan1   

  1. Shenzhen Center for Disease Control and Prevention, Shenzhen Key Laboratory of Modern Toxicology, Shenzhen 518055
  • Received:2014-05-19 Revised:2014-09-02 Online:2014-09-30 Published:2014-09-30

Abstract:

OBJECTIVE: To explore the effects of di(2-ethylhexyl) phthalate (DEHP) on hormonal-related gene expression levels in male rats. METHODS:A total of 40 healthy 5-week-old male Sprague-Dawley rats were randomly divided into four groups with 10 rats in each group. The DEHP doses were 0 mg/kg in control group(corn oil),100 mg/kg in low dose group,500 mg/kg in medium dose group and 1 500 mg/kg in high dose group. Rats were exposed to DEHP via gavage administration for six consecutive weeks,DEHP administration was once a day and five times a week. After exposure,rats were anesthetized by ether,then sacrificed for further study. The relative gene expression levels of steroidogenic acute regulatory protein (StAR),3β-hydroxysteroid dehydrogenase(3β-HSD),17β-hydroxysteroid dehydrogenase (17β-HSD),estrogen receptors (ERα/β) and gonadotropin releasing hormone (GnRH) were analyzed by real time quantitative RT-PCR. RESULTS:Compared with control group,the relative gene expression levels of StAR and 3β-HSD were increased in medium DEHP dose and high DEHP dose groups (P<0.01 or P<0.05). The relative gene expression levels of 17β-HSD,ERα and ERβ were increased in high DEHP dose group (P<0.01 or P<0.05),while the relative gene expression levels of GnRH was decreased in medium DEHP dose and high DEHP dose groups(P<0.01 or P<0.05). CONCLUSION:DEHP could cause endocrine disorder and interfere with the synthesis of male hormones in rats,ultimately leading to male reproductive dysfunction.

Key words: di(2-ethylhexyl) phthalate, steroidogenic acute regulatory protein, 3β-hydroxysteroid dehydrogenase, 17β-hydroxysteroid dehydrogenase, gonadotropin releasing hormone, estrogen receptor α, estrogen receptor β, gene expression