Abstract
Developmental exposures to bisphenol A (BPA), an estrogen receptor agonist, can disrupt development of the female reproductive tract in rodents and non-human primates. Due to an increased public knowledge of negative health effects associated with BPA exposure, BPA has begun to be phased out of many consumer products and in some cases it has been replaced with structurally similar compounds including bisphenol S (BPS). This study examined CD-1 mice exposed to a low dose of BPS during early development (200 µg/kg/day from gestational day 8 until postnatal day 19). BPS altered expression of estrogen-responsive genes in both the uterus and ovary, and induced increases in ovarian follicular development in pre-pubertal females evaluated at postnatal day 22. Prior studies have revealed that developmental exposures to environmental chemicals including BPA alter the response of animals to hormonal or carcinogen challenges experienced later in life. To evaluate whether early life exposures to BPS alter responses of females to an estrogen challenge, additional females were exposed to ethinyl estradiol from postnatal day 19 through postnatal day 21. BPS-treated females responded abnormally to this estrogen challenge, displaying heightened responses in the uterus and diminished responses in the ovary. Although additional studies are needed to characterize the mechanisms by which BPS alters the female reproductive tract, this pilot study provides evidence that a common BPA replacement chemical may have endocrine disrupting properties.
Highlights
It is widely understood that early life exposures to synthetic estrogens can induce alterations to the female reproductive tract, some of which will manifest at puberty (Crain et al, 2008; Mandrup et al, 2013; Soto, Rubin, & Sonnenschein, 2007)
One caveat that must be considered in the analysis of gene expression data is that these are evaluations of whole-organ cell lysates; because different gene expression is anticipated with different follicular stages, the changes in gene expression may be reflective of changes in follicular stage, including changes that we could not detect with our histological method
Most studies of bisphenol S (BPS) point to its estrogen receptor agonist properties (Grignard et al, 2012; Kuruto-Niwa et al, 2005; Molina-Molina et al, 2013; Vinas & Watson, 2013). Some of these studies suggest that BPS may be a more potent estrogen mimic than bisphenol A (BPA), at least for some endpoints. Considering those molecular data, previous studies showing that BPS can disrupt a range of endpoints in zebrafish and rodents (Catanese & Vandenberg, 2016; Kim et al, 2015; Kinch et al, 2015; Naderi et al, 2014), and the data we present in this manuscript, it is clear there is a need for further studies to observe additional adverse outcomes associated with BPS exposure; it is clear that the data are not supportive of safety for this replacement chemical
Summary
It is widely understood that early life exposures to synthetic estrogens can induce alterations to the female reproductive tract, some of which will manifest at puberty (Crain et al, 2008; Mandrup et al, 2013; Soto, Rubin, & Sonnenschein, 2007). A relatively large number of estrogenic endocrine disrupting chemicals (EDCs) have been identified Both controlled laboratory animal and epidemiological data suggest adverse effects on the female reproductive system as a result of early life exposures (Bergman et al, 2013; Gore et al, 2015; Hunt, Susiarjo, Rubio, & Hassold, 2009; Maffini, Rubin, Sonnenschein, & Soto, 2006; Rochester, 2013). Peretz and colleagues assessed all studies published from 2007 to 2013 that examined the impact of one xenoestrogen, bisphenol A (BPA), on the male and female reproductive systems (Peretz et al, 2014) These authors concluded that BPA induced or was associated with disturbances of the ovary, oviduct and uterus in laboratory animals, and in human epidemiology studies. Consistent effects of BPA on a number of reproductive endpoints have been shown across studies conducted in multiple laboratories, and in different species (Vandenberg, Ehrlich et al, 2013)
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