Bisphenol A prevents the synaptogenic response to estradiol in hippocampus and prefrontal cortex of ovariectomized nonhuman primates.
09/09/2008
Exposure
measurements from several countries indicate that
humans are routinely exposed to low levels of
bisphenol A (BPA), a synthetic xenoestrogen widely
used in the production of polycarbonate plastics.
There is considerable debate about whether this
exposure represents an environmental risk, based on
reports that BPA interferes with the development of
many organs and that it may alter cognitive functions
and mood. Consistent with these reports, we have
previously demonstrated that BPA antagonizes spine
synapse formation induced by estrogens and
testosterone in limbic brain areas of gonadectomized
female and male rats. An important limitation of
these studies, however, is that they were based on
rodent animal models, which may not be representative
of the effects of human BPA exposure. To address this
issue, we examined the influence of continuous BPA
administration, at a daily dose equal to the current
U.S. Environmental Protection Agency's reference safe
daily limit, on estradiol-induced spine synapse
formation in the hippocampus and prefrontal cortex of
a nonhuman primate model. Our data indicate that even
at this relatively low exposure level, BPA completely
abolishes the synaptogenic response to estradiol.
Because remodeling of spine synapses may play a
critical role in cognition and mood, the ability of
BPA to interfere with spine synapse formation has
profound implications. This study is the first to
demonstrate an adverse effect of BPA on the brain in
a nonhuman primate model and further amplifies
concerns about the widespread use of BPA in medical
equipment, and in food preparation and storage.
Proc Natl Acad Sci U S A. 2008 Sep 3. [Epub ahead of print]
Proc Natl Acad Sci U S A. 2008 Sep 3. [Epub ahead of print]
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