June 11, 2009 — New research by a team of scientists
at the University of Cincinnati (UC) shows thatbisphenol A (BPA) may be harmful for the heart,particularly in women.
Results of several studies are being presented inWashington, D.C., at ENDO 09, the Endocrine Society'sannual meeting, June 10-13.
A research team lead by Scott Belcher, PhD, HongSheng Wang, PhD, and Jo El Schultz, PhD, in thedepartment of pharmacology and cell biophysics, foundthat exposure to BPA and/or estrogen causes abnormalactivity in hearts of female rats and mice.
In addition, these researchers found that estrogenreceptors are responsible for this affect in heart musclecells.
"There is broad exposure to bisphenol A, despiterecognition that BPA can have harmful effects,"Belcher says. "We had reason to believe that harmfulcardiovascular affects can be added to the list."
BPA, an environmental pollutant with estrogen activity,is used to make hard, clear plastic and is common in
Bisphenol A (BPA), found in many plastics,
many food product containers. It has been linked to
may be harmful for the heart, particularly in
neurological defects, diabetes and breast and prostate
women. (Credit: iStockphoto/Fred Goldstein)
Using live cultures of cells isolated from rat or mouse hearts, researchers briefly exposed the cardiac cellsto BPA and/or estrogen. Both compounds caused striking changes in the activity of cardiac muscle cellsfrom females but not males. Additional studies revealed that these cellular changes in activity causedimproperly controlled beating in the female heart.
"Low doses of BPA markedly increased the frequency of arrhythmic events," Belcher says. "The effect ofBPA on these cardiac arrhythmias was amplified when exposed to estradiol, the major estrogen hormonein humans."
The mechanism underlying this harmful effect was investigated using cellular imaging techniques.
"BPA and/or estrogen rapidly stimulated contraction by altering control of the concentrations of freecalcium inside the heart cell but only in heart muscle cells from females, showing that these effects weresex-specific," Belcher says. "BPA's presence increased the frequency of calcium 'sparks' from the
sarcoplasmic reticulum—the part of the cardiac muscle that stores and releases calcium ions—indicatingspontaneous release or 'leak' that's likely causing the heart arrhythmias and may have other harmfulactions, especially following heart attack."
Belcher and colleagues also investigated the nature of the mechanisms that mediated the responses of thecardiac muscle cells to estrogen and BPA.
"Pharmacological studies using selective estrogen receptor drugs and animal models lacking estrogenreceptors were used to investigate the role of each estrogen receptor in mediating the rapid sex-specificfunction effects of E2 and BPA in cells," he says. "Our findings suggest that estrogen has opposing actionsin cardiac cells.
"In female cardiac muscle cells, the blocking or genetic removal of estrogen receptor beta completelyblocked the contractile effects of BPA and estrogen, while in males, blockade of the effects of estrogenreceptor alpha caused the male heart to become more 'female-like' and become responsive to estrogen andBPA.
"These studies have identified new and important potential cardiac risks associated with BPA exposurethat may be especially important for women's heart health," he says.
This study was funded by grants from the National Institutes of Health and the UC Center forEnvironmental Genetics.
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