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高黄油脂肪饮食和双酚A会叠加损害雄性大鼠的精子发生。

High butter-fat diet and bisphenol A additively impair male rat spermatogenesis.

作者信息

Tarapore Pheruza, Hennessy Max, Song Dan, Ying Jun, Ouyang Bin, Govindarajah Vinothini, Leung Yuet-Kin, Ho Shuk-Mei

机构信息

Department of Environmental Health, University of Cincinnati Medical Center, Cincinnati, OH, USA; Center for Environmental Genetics, University of Cincinnati Medical Center, Cincinnati, OH, USA; Cincinnati Cancer Center, Cincinnati, OH, USA.

Department of Environmental Health, University of Cincinnati Medical Center, Cincinnati, OH, USA.

出版信息

Reprod Toxicol. 2017 Mar;68:191-199. doi: 10.1016/j.reprotox.2016.09.008. Epub 2016 Sep 19.

Abstract

Exposure to xenoestrogens is a probable cause of male infertility in humans. Consumption of high-fat diets and exposure to bisphenol A (BPA) is pervasive in America. Here, we test the hypothesis that gestational exposure to high dietary fats and/or BPA disrupt spermatogenesis in adulthood. Sprague-Dawley rats were fed diets containing 10kcal% butter fat (AIN), 39kcal% butter fat (HFB), or 39kcal% olive oil (HFO), with or without BPA (25μg/kg body weight/day) during pregnancy. One group of male offspring received testosterone (T)- and estradiol-17β (E2)-filled implants or sham-implants from postnatal day (PND)70-210. Another group was naturally aged to 18 months. We found that adult males with gestational exposure to BPA, HFB, or HFB+BPA, in both the aged group and the T+E2-implanted group, exhibited impairment of spermatogenesis. In contrast, gestational exposure to HFO or HFO+BPA did not affect spermatogenesis. Sham-implanted, gestational exposed groups also had normal spermatogenesis. Loss of ERα expression in round spermatids and premature expression of protamine-1 in diplotene spermatocytes were features associated with impaired spermatogenesis. Compared with the single-treatment groups, the HFB+BPA group experienced more severe effects, including atrophy.

摘要

接触外源性雌激素可能是人类男性不育的一个原因。在美国,高脂肪饮食的摄入和双酚A(BPA)的接触非常普遍。在此,我们检验这样一个假设:孕期接触高脂肪饮食和/或双酚A会破坏成年期的精子发生。将斯普拉格-道利大鼠在孕期喂食含10千卡%乳脂(AIN)、39千卡%乳脂(HFB)或39千卡%橄榄油(HFO)的饮食,且部分大鼠在孕期接触或不接触双酚A(25微克/千克体重/天)。一组雄性后代从出生后第70天至210天接受填充睾酮(T)和雌二醇-17β(E2)的植入物或假植入物。另一组自然老化至18个月。我们发现,在老年组和T+E2植入组中,孕期接触双酚A、HFB或HFB+BPA的成年雄性均表现出精子发生受损。相比之下,孕期接触HFO或HFO+BPA并不影响精子发生。假植入的孕期暴露组精子发生也正常。圆形精子细胞中ERα表达缺失以及双线期精母细胞中鱼精蛋白-1过早表达是与精子发生受损相关的特征。与单一处理组相比,HFB+BPA组受到的影响更严重,包括萎缩。

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