Induction of spermatogenic cell apoptosis in prepubertal rat testes irrespective of testicular steroidogenesis: a possible estrogenic effect of di(n-butyl) phthalate
Induction of spermatogenic cell apoptosis in prepubertal rat testes irrespective of testicular steroidogenesis: a possible estrogenic effect of di(n-butyl) phthalate
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DOI：
10.1530/rep-09-0226
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发表时间：
2010-02-01
期刊：
影响因子：
3.8
通讯作者：
Kurohmaru, Masamichi
中科院分区：
文献类型：
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作者：
Alam, Mohammad Shah;Ohsako, Seiichiroh;Kurohmaru, Masamichi
虽然邻苯二甲酸二丁酯（DBP），一种可疑的内分泌干扰物，诱导青春期前雄性大鼠睾丸萎缩，它是否在体内发挥雌激素活性仍然是一个争论的问题。在本研究中，我们探讨了DBP的雌激素效力使用3周龄雄性大鼠，然后检查雌激素诱导的生精细胞凋亡和睾丸类固醇生成之间的关系。每日暴露于DBP 7天，导致睾丸萎缩，由于生精细胞的损失，而睾丸类固醇生成几乎与对照值相同。一个单一的暴露DBP降低睾丸类固醇生成，除了降低血清LH水平DBP治疗后3小时，与一个非常高的发生率凋亡的生精细胞在6小时后给药。为了阐明DBP的雌激素活性，我们在DBP或雌二醇-3-苯甲酸酯（EB）诱导的生精细胞凋亡模型中使用纯抗雌激素ICI 182，780（10）进行了抑制研究。虽然DBP和EB处理组的生精细胞凋亡显着增加，ICI预处理显着减少这两组中的生精细胞凋亡的数量。相反，睾丸类固醇生成和血清FSH在所有治疗组中显著降低，甚至在DBP + ICI和EB + ICI组中也是如此。两者合计，这些研究结果使我们得出结论，雌激素化合物，如DBP和EB诱导生精细胞凋亡在青春期前大鼠，可能通过激活睾丸中的雌激素受体，并减少睾丸类固醇激素合成功能诱导的雌激素化合物与生精细胞凋亡无关。生殖（2010年）139 427-437
Although di(n-butyl) phthalate (DBP), a suspected endocrine disruptor, induces testicular atrophy in prepubertal male rats, whether it exerts estrogenic activity in vivo remains a matter of debate. In the present study, we explored the estrogenic potency of DBP using 3-week-old male rats, and then examined the relationship between estrogen-induced spermatogenic cell apoptosis and testicular steroidogenesis. Daily exposure to DBP for 7 days caused testicular atrophy due to loss of spermatogenic cells, whereas testicular steroidogenesis was almost the same with the control values. A single exposure of DBP decreased testicular steroidogenesis in addition to decreasing the level of serum LH at 3 h after DBP treatment, with an extremely high incidence of apoptotic spermatogenic cells at 6 h after administration. To elucidate the estrogenic activity of DBP, we carried out an inhibition study using pure antiestrogen ICI 182,780 (10) in a model of spermatogenic cell apoptosis induced by DBP or estradial-3-benzoate (EB). Although both the DBP- and EB-treated groups showed a significant increase in spermatogenic cell apoptosis, ICI pretreatment significantly decreased the number of apoptotic spermatogenic cells in these two groups. In contrast, testicular steroidogenesis and serum FSH were significantly reduced in all the treated groups, even in the DBP + ICI and EB + ICI groups. Taken together, these findings led us to conclude that estrogenic compounds such as DBP and EB induce spermatogenic cell apoptosis in prepubertal rats, probably by activating estrogen receptors in testis, and that reduction in testicular steroidogenic function induced by estrogenic compounds is not associated with spermatogenic cell apoptosis. Reproduction (2010) 139 427-437