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邻苯二甲酸二(2-乙基己基)酯致胎鼠隐睾发生过程中胰岛素样因子3的表达分析 被引量:4

Effect of Di-(2-ethylhexyl)Phthalate on Insulin Like Factor 3 Expression in Fetal Mice
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摘要 目的:探讨环境内分泌干扰物邻苯二甲酸二(2-乙基已基)酯[Di-(2-ethylhexyl)phthalate,DEHP]诱发胎鼠隐睾的分子机制。方法:妊娠昆明小鼠随机分为3组,每组15只:DEHP实验组(A组)、玉米油(溶剂)对照组(B组)和正常对照组(C组)。A组和B组自妊娠12.5 ̄18.5d分别持续经口每天给予DEHP(500mg/kg)或玉米油,C组不予灌药。结果:B组和C组睾丸组织中胰岛素样因子3(INSL3)mRNA和蛋白质的表达均无差异(P>0.05);A组INSL3mRNA的表达量约为B或C组的1/3,INSL3蛋白质的表达量约为B或C组的1/4,与B或C组比其差异显著(P<0.05)。A组睾丸引带发育不良,睾丸位置异常。结论:环境内分泌干扰物DEHP下调睾丸间质细胞INSL3基因的表达,影响睾丸引带发育,可能是DEHP诱发隐睾的分子机制之一。 Objective:To explore the molicular mechanism of cryptorchidism induced by Di-(2-ethylhexyl)phthalate(DEHP)in mice.Methods:Kunming mice were divided into 3 groups randomly with 15 in each group:DEHP-exposed group(group A),corn oil(menstrum)group(group B)and normal control group(group C).Group A or group B was administered respectively with DEHP(500 mg/kg)or corn oil to the pregnant mice from gestation day 12.5(GD12.5)to 18.5,and group C with nothing.Results:DEHP altered gubernacular development,disrupted testis decent,and induce cryptorchidism.MRNA and protein expression of INSL3 between groups B and C were not significant(P0.05).INSL3 mRNA expression in group A was about one-third of that in group C,which was significantly decreased(P0.05).Similarly,INSL3 protein expression in DEHP-exposed group was about quarter of that in group A,which was also significantly decreased(P0.05).In group C,the development of gubernaculum was not well and the site of testis was abnormal.Conclusion:DEHP as one of environmental endocrine disruptors,can down-regulate INSL3 gene expression and interfere the gubernaculum development.It may be one of possible mechanisms that DEHP cause cryptorchidism.
出处 《生殖与避孕》 CAS CSCD 北大核心 2009年第8期502-507,共6页 Reproduction and Contraception
基金 国家自然科学基金(30872706) 重庆市自然科学基金(2007BB5325)项目
关键词 环境内分泌干扰物 邻苯二甲酸二(2-乙基已基)酯 胰岛素样因子3 隐睾 environmental endocrine disruptors Di-(2-ethylhexyl)phthalate(DEHP) insulin like factor 3(INSL3) cryptorchidism
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参考文献21

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二级参考文献11

  • 1王炜,魏光辉,邓永继.环境内分泌干扰因子DEHP与隐睾发病相关性的实验研究[J].中华小儿外科杂志,2004,25(6):70-74. 被引量:16
  • 2Mahood IK, Hallmark N, McKinnell C, et al. Abnormal Leydig cell aggregation in the fetal testis of rats exposed to di (n-butyl) phthalate and its possible role in testicular dysgenesis.Endocrinology, 2005, 146(2):613-23.
  • 3Barlow NJ & Foster PM. Pathogenesis of male reproductive tract lesions from gestation through adulthood following in utero exposure to Di(n-butyl) phthalate. Toxicol Pathol,2003, 31(4):397-410.
  • 4Koch HM, Preuss R & Angerer J. Di(2-ethylhexyl)phthalate (DEHP): human metabolism and internal exposure - an update and latest results. Int J Androl, 2006, 29(1):155-65.
  • 5Chael Joffe. Are problems with male reproductive health caused by endocrine disruption? Occup Environ Med, 2001,58(4):281-8.
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  • 7Emmen JM, McLuskey A, Adham IM, et al. Hormonal control of gubemaculums development during testis descent:gubernaculum outgrowth in vitro requires both insulin-like factor and androgen. Endocrinology, 2000, 141 (12):4 720-7.
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  • 9Bogatcheva NV, Truong A, Feng S, et al. GREAT/LGR8 is the only receptor for insulin-like 3 peptide. Mol Endocrinol,2003, 17(12):2 639-46.
  • 10Tomiyama H, Hutson JM, Truong A, et al. Transabdominal testicular descent is disrupted in mice with deletion of insulin like factor 3 receptor. J Pediatr Surg, 2003, 38(12):1 793-8.

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