2001
DOI: 10.1016/s0304-3940(01)02092-4
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Bisphenol-A differently affects estrogen receptors-α in estrous-cycling and lactating female rats

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Cited by 68 publications
(29 citation statements)
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“…A study of nonpregnant or lactating Sprague-Dawley rats examined the effects of high doses of BPA (40 mg/kg/d) on ERa immunoreactive cells in the MPOA, ventromedial hypothalamus, and arcuate nucleus. Although lactating females had fewer ERa-expressing cells in the MPOA compared with nonlactating females, there were no significant effects of BPA in the lactating group (86). Here, the response to BPS we observed in the MPOA in F0 females supports the idea that pregnancy/lactation represents a vulnerable period for exposures and that the effects may be "activational" (e.g., only occurring during the period of exposure) (87)(88)(89).…”
Section: Discussionsupporting
confidence: 72%
“…A study of nonpregnant or lactating Sprague-Dawley rats examined the effects of high doses of BPA (40 mg/kg/d) on ERa immunoreactive cells in the MPOA, ventromedial hypothalamus, and arcuate nucleus. Although lactating females had fewer ERa-expressing cells in the MPOA compared with nonlactating females, there were no significant effects of BPA in the lactating group (86). Here, the response to BPS we observed in the MPOA in F0 females supports the idea that pregnancy/lactation represents a vulnerable period for exposures and that the effects may be "activational" (e.g., only occurring during the period of exposure) (87)(88)(89).…”
Section: Discussionsupporting
confidence: 72%
“…This could be explained by a different affinity of BPA (with respect to estradiol) with estrogen α-receptors (8) and β-receptors (20,21). Our previous experiments have demonstrated that exposure of female rats in adulthood to BPA at the same dosage as in the present experiment, modifies the number of estrogen α-receptors in the brain, thus proving an effect on the central nervous system (22).…”
Section: Discussionsupporting
confidence: 49%
“…Moreover, differential promoter activity has been shown to be a key regulator of tissue-specific ERa expression (Kato et al 1998, Donaghue et al 1999. Here, we suggest that the alternative promoter usage of the ERa gene is regulated by BPA exposure in a dose-sensitive manner and therefore this mechanism could be, at least in part, responsible for the different and sometimes contradictory effects observed in BPA action on gene transcription (Khurana et al 2000, Kwon et al 2000, Aloisi et al 2001, Ramos et al 2003, Patisaul et al 2006. Since sexual differentiation of the hypothalamus is estrogen-dependent and mediated at least partly through ERa (Simerly et al 1997), BPA deregulation of this receptor could affect the natural estrogen-directed dimorphisms of POA circuits.…”
Section: Discussionmentioning
confidence: 76%