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

Reprod Toxicol

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; Cincinnati Veteran Affairs Hospital Medical Center, Cincinnati, OH, USA. Electronic address:

Published: March 2017

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.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5357593PMC
http://dx.doi.org/10.1016/j.reprotox.2016.09.008DOI Listing

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