Metabolic response to chronic bisphenol A exposure in C57bl/6n mice

Patel, Bhavini; Iorio, Massimo Di; Chalifour, Lorraine E.

doi:10.1016/j.toxrep.2014.07.012

Cited by 18 publications

(26 citation statements)

References 56 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…On the other hand concentration of total cholesterol, both free and bound, has been increased in exposed groups of rats in our study. Similar findings have been reported, in case of BPA exposure [36] , [37] . BPS might increase the cholesterol concentration by inducing the peripheral cholesterol biosynthesis, increasing the degeneration of cell membranes in the process of cell apoptosis, and/or decreasing the level of HDL lipoprotein which carries cholesterol from dying cells to the liver for excretion.…”

Section: Discussionsupporting

confidence: 91%

Bisphenol S impairs blood functions and induces cardiovascular risks in rats

et al. 2017

View full text Add to dashboard Cite

show abstract

Section: Discussionsupporting

confidence: 91%

Bisphenol S impairs blood functions and induces cardiovascular risks in rats

et al. 2017

View full text Add to dashboard Cite

show abstract

“…Supporting the epidemiological results, early life exposure to BPA or the estrogenic compound diethylstilbestrol (DES) in mice and rats was correlated with increased body size and body weight in the adult progeny [26] , [38] , [51] , [60] . In contrast, chronic exposure to BPA did not lead to increased body size [30] , [42] .…”

Section: Introductionmentioning

confidence: 74%

Sex-specific cardiovascular responses to control or high fat diet feeding in C57bl/6 mice chronically exposed to bisphenol A.

et al. 2015

Self Cite

View full text Add to dashboard Cite

The increased pericardial fat which often accompanies overall obesity is thought to alter cardiac structure/function and increase the risk for atrial fibrillation. We hypothesized that chronic exposure to bisphenol A (BPA) would induce pericardial fat, cardiac hypertrophy or arrhythmia. C57bl/6n dams were exposed to BPA (25 ng/ml drinking water) beginning on gestation day 11 and progeny continued on 2.5 ng BPA/ml drinking water. The progeny of control dams (VEH) and dams treated with diethylstilbestrol (DES, 1 μg/kg/day, gestation days 11⿿14) had tap water. After weaning progeny were fed either a control (CD) or high fat diet (HFD) for 3 months. Pericardial fat was present in CD-BPA and CD-DES and not CD-VEH mice, and was increased in all HFD mice. Catecholamine challenge revealed no differences in males, but BPA-exposed females had longer P-wave and QRS complex duration. Only CD-BPA and CD-DES females developed cardiac hypertrophy which was independent of increased blood pressure. Calcium homeostasis protein expression changes in HFD-BPA and HFD-DES mice predict reduced SERCA2 activity in males and increased SERCA2 activity in females. Thus, chronic BPA exposure induced pericardial fat in the absence of HFD, and female-specific changes in cardiac hypertrophy development and cardiac electrical conduction after a catecholamine challenge.

show abstract

“…In mouse models of myocardial infarctions several studies found chronic BPA exposure worsened outcomes 14–16 . Furthermore, laboratory animal studies consistently show acute 5,17 and life-long 18,19 exposure of BPA at doses within the ranges seen in human populations has pro-arrhythmic effects. Studies showing negative cardiovascular effects of BPA exposure are particularly concerning given the widespread inclusion of BPA in medical devices which increase the levels in patients who are already at greater risk for cardiovascular complications 20 .…”

Section: Introductionmentioning

confidence: 92%

Bisphenol S rapidly depresses heart function through estrogen receptor-β and decreases phospholamban phosphorylation in a sex-dependent manner

Ferguson

Lorenzen‐Schmidt

Pyle

2019

Sci Rep

View full text Add to dashboard Cite

The health effects of the endocrine disruptor Bisphenol A (BPA) led to its partial replacement with Bisphenol S (BPS) in several products including food containers, toys, and thermal paper receipts. The acute effects of BPS on myocardial contractility are unknown. We perfused mouse hearts from both sexes for 15 min with physiologically relevant doses of BPS or BPA. In females BPS (1 nM) decreased left ventricular systolic pressure by 5 min, whereas BPA (1 nM) effects were delayed to 10 min. BPS effects in male mice were attenuated. In both sexes ER-β antagonism abolished the effects of BPS. Cardiac myofilament function was not impacted by BPS or BPA in either sex, although there were sex-dependent differences in troponin I phosphorylation. BPS increased phospholamban phosphorylation at S16 only in female hearts, whereas BPA reduced phosphorylation in both sexes. BPA decreased phospholamban phosphorylation at T17 in both sexes while BPS caused dephosphorylation only in females. This is the first study to compare sex differences in the acute myocardial response to physiologically relevant levels of BPS and BPA, and demonstrates a rapid ability of both to depress heart function. This study raises concerns about the safety of BPS as a replacement for BPA.

show abstract

Metabolic response to chronic bisphenol A exposure in C57bl/6n mice

Cited by 18 publications

References 56 publications

Bisphenol S impairs blood functions and induces cardiovascular risks in rats

Bisphenol S impairs blood functions and induces cardiovascular risks in rats

Sex-specific cardiovascular responses to control or high fat diet feeding in C57bl/6 mice chronically exposed to bisphenol A.

Bisphenol S rapidly depresses heart function through estrogen receptor-β and decreases phospholamban phosphorylation in a sex-dependent manner

Contact Info

Product

Resources

About