Many reports describe an association between preconceptional paternal exposure to environmental chemicals, including the persistent organic pollutant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) with an increased number of female offspring. We chronically treated wild-type C57BL/6 male mice with TCDD to investigate a role for the aryl hydrocarbon receptor (AHR) transcription factor. These mice had a 14 % lower male:female sex ratio than control mice, which was not observed in TCDD-treated Ahr knock out mice. AHR target genes Cyp1a1 and Ahrr were upregulated in the liver and testis of WT mice and Ahr expression was higher in the epididymis (2-fold) and liver (18-fold) than in whole testis tissue. The AHR protein was localized to round spermatids, elongating spermatids, and Leydig cells in the testis of WT mice. These studies demonstrate AHR involvement in the sex ratio distortion of TCDD-exposed males and the need for evaluating the molecular and genetic mechanism of this process.

中文翻译：

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芳基碳氢化合物受体介导暴露于TCDD的雄性小鼠胚胎的性别比例畸变。

许多报告描述了受孕前父亲暴露于环境化学品中，包括持久性有机污染物2,3,7,8-四氯二苯并-对-二恶英（TCDD）与女性后代数量增加之间的联系。我们用TCDD对野生型C57BL / 6雄性小鼠进行了长期治疗，以研究其对芳烃受体（AHR）转录因子的作用。这些小鼠的性别比例比对照小鼠低14％，这在TCDD处理的Ahr基因敲除小鼠中未观察到。WT小鼠肝脏和睾丸中的AHR靶基因Cyp1a1和Ahrr上调，附睾和肝脏中Ahr的表达高于整个睾丸组织的2倍（18倍）。AHR蛋白定位于WT小鼠睾丸中的圆形精子细胞，延伸的精子细胞和Leydig细胞。