Stressor: 521
Title
Bisphenol A
Stressor Overview
AOPs Including This Stressor
Events Including This Stressor
Chemical Table
| User term | DTXID | Preferred name | Casrn | jchem_inchi_key | indigo_inchi_key |
|---|---|---|---|---|---|
| Bisphenol A | DTXSID7020182 | Bisphenol A | 80-05-7 | IISBACLAFKSPIT-UHFFFAOYSA-N | IISBACLAFKSPIT-UHFFFAOYSA-N |
AOP Evidence
Binding to estrogen receptor (ER)-α in immune cells leading to exacerbation of systemic lupus erythematosus (SLE)
There is no evidence text for this AOP
Event Evidence
Binding to estrogen receptor (ER)-α in immune cells
There is no evidence text for this event.
Induction of GATA3 expression
GATA3 expression is induced in Th cells primed by dendritic cells exposed to BPA (Guo H. 2010). Purified naive T cells were cultured and expanded under Th1 culture conditions in the presence or absence of 0.3 μM 4-HT (Research Biochemicals Institute) for 2 weeks starting from days 1, 7, 14, or 21 (Kurata H. 1999).
Increase of Th2 cells producing IL-4
Mouse lymphocytes stimulated with a massive amount of BPA (50 μM) were Th2 polarized, with prominent elevation of IL-4 as well as IL-10 (Lee J. 2010). Similarly, BPA enhanced IL-4 production in antigen-activated T cells by ELISA or RT-PCR, although the concentrations of BPA that they utilized (10-50 μM) were high (Lee MH. 2003). In this experiment, IL-4 level is confirmed baseline when treated with anti-CD4 mAb. Exposure to BPA in adulthood mice promoted antigen-stimulated levels of IL-4, IL-10, and IL-13, but not IFN-γ (Huimin Y. 2008).
Increase of anti-DNA antibody from autoreactive B cell
BPA as well as E2 and diethylstilbestrol (DES) enhanced anti-Br-RBC autoantibody production by B1 cells in vivo. IgM production by B1 cells in the presence of ED was more prominent on aged BWF1 mice developing lupus nephritis. (Yurino H. 2004).
In a murine model of SLE, BPA increased the number of B cells producing autoantibodies, and IgM antibody secretion by B1 cells was augmented (Yurino H. 2004).
To examine a direct effect of endocrine disruptors on IgM antibody production by B1 or B2 cells, B1 cells were prepared from peritoneal cells and B2 cells from spleen, B1 or B2 cells were cultured in the presence of endocrine disruptors (E2: 100 nM, DES: 100 nM, BPA: 1 μM) for 4 days (Yurino H. 2004).
Exacerbation of systemic lupus erythematosus (SLE)
There is no evidence text for this event.
Disrupted meiotic initiation of fetal oogonia of the ovary
Bisphenol A (BPA) exposure may delay entry into meiotic prophase I in mice, potentially through reduced Stra8 expression (Zhang et al, 2012). This effect from BPA exposure was not seen in a second mouse study (Lawson et al, 2011), nor in human ovary explant cultures (Brieño-Enríquez et al, 2012). As such, it remains uncertain if BPA can prevent oocytes from entering meiosis.
Reduced size of the ovarian follicle pool
Bisphenol A (BPA) exposure during the postnatal period (20 mg/kg, s.c., 1, 3, 5, and 7 dpp, killen on 8 dpp) reduced the number of primordial follicles in rats exposed postnatally (Rodríguez et al. 2010). In mice exposed exposed to BPA during fetal life (0.5 and 50 µg/kg/day, oral, 11 dpc-birth, killed on 4 dpp) reduced number of primordial follicles were seen (Wang et al. 2014). Reduced number of primordial follicles was also seen in mice exposed during a shorter window of time during fetal life (0.08mg/kg, oral, 12.5-18.5 dpc, killed 15.5, 17.5 and 19.5 dpc and 3, 5 and 7 dpp (Zhang et al. 2012).
Increased (ectopic) all-trans retinoic acid concentration
Bisphenol A, an organic synthetic compound used to make polycarbonate plastic. In mice, BPA exposure increased levels of atRA and expression of RA biosynthesis enzymes (incl Adh1 and Cyp1a2) (Esteban et al, 2019).