Study: Byproduct of BPA May Cause Most Damage
The finding could lead to development drugs to resolve the problem
Thursday, October 11, 2012
A debate continues over the use of Bisphenol A (BPA) in food containers and other plastic consumer products, but new research suggests it's not the BPA, but a metabolic by-product, that is the major cause for concern.
The food industry favors BPA because it is the chemical that makes plastic rigid and more suitable for food containers. It's often used as a liner in food cans.
But health officials point to numerous studies that show BPA is easily transferred to the human body and, once there, can cause health problems. Of primary concern is BPA's impact on the human reproductive system.
In a study published in 2002, researchers discovered that exposure to estrogenic compounds, such as BPA, during critical periods of fetal development could result in adverse effects on the development of reproductive organs which do not become apparent until later in life.
In new research published in the October 4 online issue of the journal PLOS ONE, two scientists at University of California San Diego School of Medicine say three-dimensional modeling suggests a metabolite of BPA -- a molecule produced when BPA is metabolized or broken down by the body -- actually causes the problem. They say it binds to the estrogen receptor much more strongly than BPA itself.
The finding could point the way to development of a new class of drugs designed to specifically inhibit excessive estrogen activity linked to disease.
According to Michael E. Baker, PhD, UCSD professor of medicine, and Charlie Chandsawangbhuwana, a graduate student in the UCSD Department of Bioengineering, several research labs have reported that BPA binds weakly to the estrogen receptor, suggesting that something else is interacting with this receptor and causing the problem.
A 2004 study found that a compound called MBP is produced when BPA is metabolized. MBP has a 100 to 1000 times stronger bond to the estrogen receptor than BPA. However, the structural basis for MBP’s high affinity for the estrogen receptor was not investigated further.
In their study Baker and Chandsawangbhuwana found that BPA actually has a fairly weak hold on the estrogen receptor, but its byproduct is practically fused to it.
“In other words, MBP is basically grabbing onto the estrogen receptor with two hands compared to just one hand for BPA,” said Baker. “Two contact points makes a much stronger connection.”
Baker said the 3D modeling supports the idea that BPA is not the endocrine disruptor culprit. Instead, MBP is one of perhaps several BPA metabolites that causes disruption of estrogen signaling in humans and other animals.
He said that means research needs to measure MBP levels in urine and blood of patients suspected of BPA-mediated health effects. The findings, he says, may fuel development of a new therapeutic treatment for conditions linked to excessive estrogen levels and activity, such as some forms of breast and prostate cancers.
More than 90 percent of all Americans are believed to carry varying levels of BPA exposure.
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