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首页> 外文期刊>Reproductive toxicology >Fetal testosterone insufficiency and abnormal proliferation of Leydig cells and gonocytes in rats exposed to di(n-butyl) phthalate.
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Fetal testosterone insufficiency and abnormal proliferation of Leydig cells and gonocytes in rats exposed to di(n-butyl) phthalate.

机译：胎儿邻苯二甲酸二正丁酯对大鼠睾丸功能不全和Leydig细胞和生殖细胞的异常增殖。

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Adult male rats previously exposed on gestation days (GD) 12-21 to di(n-butyl) phthalate (DBP) have reproductive tract malformations, particularly agenesis of the epididymis, decreased sperm production, and Leydig cell hyperplasia and adenomas. Although similar effects are produced by the potent androgen receptor (AR) antagonist flutamide and are indicative of disruption of male sexual differentiation via an antiandrogenic mechanism, DBP is not an AR antagonist. The purpose of the study was to determine whether DBP causes pathologic changes and alterations in androgen status in the testis during the prenatal period of male reproductive tract differentiation. Pregnant CD rats were given corn oil, DBP (500 mg/kg/day), or flutamide (100 mg/kg/day) p.o. on GD 12-21. At GD 16-21, DBP caused hyperplasia of Leydig cells, many of which were 3beta-hydroxysteroid dehydrogenase- and/or AR-positive. Focal areas of hyperplasia had increased numbers of Leydig cells positive for proliferating cell nuclear antigen (PCNA). At GD 21, testis atrophy was apparent, seminiferous cords in DBP-exposed fetuses were enlarged and contained multinucleated gonocytes that, unlike controls, were PCNA-positive. DBP, but not flutamide, markedly decreased testicular testosterone levels at GD 18 and 21. Fewer epididymal ducts and reduced AR staining in some ducts were evident with DBP treatment, whereas decreased overall AR staining was seen with flutamide in the presence of mild Leydig cell hyperplasia. Leydig cell proliferation is likely a compensatory mechanism to increase testicular steroidogenesis triggered by testosterone insufficiency. The overall decrease in androgen concentration is not corrected and results in reproductive tract malformations. The multinuclearity and proliferation of gonocytes suggests an underlying Sertoli cell dysfunction.
机译：先前在妊娠日（GD）12-21暴露于邻苯二甲酸二正丁酯（DBP）的成年雄性大鼠生殖道畸形，特别是附睾发育不良，精子生成减少以及Leydig细胞增生和腺瘤。尽管有效的雄激素受体（AR）拮抗剂氟他胺产生了相似的效果，并且表明通过抗雄激素机制破坏了男性的性别分化，但DBP并不是AR拮抗剂。这项研究的目的是确定在男性生殖道分化的产前时期，DBP是否会引起睾丸的病理变化和雄激素状态改变。怀孕的CD大鼠口服p.o玉米油，DBP（500 mg / kg /天）或氟他胺（100 mg / kg /天）。在GD 12-21上。在GD 16-21，DBP引起Leydig细胞增生，其中许多是3β-羟类固醇脱氢酶和/或AR阳性。增生的病灶区域增加了对增殖细胞核抗原（PCNA）呈阳性的Leydig细胞的数量。在GD 21时，睾丸萎缩明显，暴露于DBP的胎儿中的生精索增大，并含有多核细胞，与对照组不同，它们是PCNA阳性的。 DBP处理可显着降低GD 18和21时睾丸睾丸激素水平，而氟他胺则不明显。DBP治疗可明显减少附睾导管，某些导管中的AR染色减少，而在轻度Leydig细胞增生的情况下，使用flutamide可使整体AR染色减少。 。睾丸间质细胞增殖可能是一种补充机制，可增加由睾丸激素不足引起的睾丸类固醇生成。雄激素浓度的总体下降未得到纠正，并导致生殖道畸形。生殖细胞的多核和增殖表明潜在的支持细胞功能障碍。

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