The xenoestrogens ethinylestradiol and bisphenol A regulate BCRP at the blood-brain barrier of rats
1. Breast cancer resistance protein (BCRP) is an ABC-transporter at the blood-brain barrier (BBB) facilitating efflux of xenobiotics into blood. Expression and function are regulated via estrogen-receptors (ERs).2. 17α-Ethinylestradiol (EE2) and bisphenol A (BPA) represent two prominent xenoestrogen...
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| Main Authors: | , |
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| Format: | Article (Journal) |
| Language: | English |
| Published: |
19 Jun 2014
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| In: |
Xenobiotica
Year: 2014, Volume: 44, Issue: 11, Pages: 1046-1054 |
| ISSN: | 1366-5928 |
| DOI: | 10.3109/00498254.2014.922226 |
| Online Access: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.3109/00498254.2014.922226
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| Author Notes: | Sabrina Nickel, Anne Mahringer |
MARC
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| 520 | |a 1. Breast cancer resistance protein (BCRP) is an ABC-transporter at the blood-brain barrier (BBB) facilitating efflux of xenobiotics into blood. Expression and function are regulated via estrogen-receptors (ERs).2. 17α-Ethinylestradiol (EE2) and bisphenol A (BPA) represent two prominent xenoestrogens. We studied whether EE2 and BPA regulate BCRP function and expression upon a 6 h treatment in an ER-dependent manner in a rat BBB-ex-vivo-model.3. Isolated brain capillaries were incubated with EE2 or BPA. BCRP function and expression were analyzed by confocal microscopy and Western-Blot. ERα-antagonist MPP and ER-antagonist ICI182.780 were used to study involvement of ERs.4. EE2 and BPA down-regulated BCRP transport function and expression. EE2 effects occurred at pharmacologically relevant doses, BPA exhibited only weak influences. Down-regulation by EE2 was reversed by ICI but not MPP. BPA effects were not reversed by either antagonist.5. EE2 is a potent regulator of BCRP expression and function acting by ERβ-stimulation. Oral contraception could alter uptake of pharmaceuticals to the brain and might thus be considered as an origin of central nervous system (CNS) side-effects. EE2 could also present a novel co-treatment to improve CNS-pharmacotherapy. BPA is a weak modulator of BCRP expression. Its effects appear not to be caused by ERs. | ||
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