Duke University researchers have identified the mechanism by which bisphenol A (BPA) allegedly affects nervous system development by suppressing a gene “vital to nerve cell function,” according to a February 25, 2013, press release. Michele Yeo, et al., “Bisphenol A delays the perinatal chloride shift in cortical neurons by epigenetic effects on the Kcc2 promoter,” PNAS, February 2013. The study focused on cortical neuron development, during which time a protein called Kcc2 expels chloride ions that would otherwise “damage neural circuits and compromise the nerve cell’s ability to migrate to its proper position in the brain.”

Using cell cultures from rats and humans, researchers purportedly found that
BPA suppresses the gene responsible for Kcc2 production, raising concerns
about whether BPA “could contribute to neurodevelopmental disorders such
as Rett syndrome, a severe autism spectrum disorder found only in girls…
[and] characterized by mutations in the gene that produces MECP2.” When
exposed to BPA, this latter protein evidently becomes “more abundant and
binds to the Kcc2 gene at a higher rate, which might help to shut it down.”

“Overall, our results indicate that BPA can disrupt Kcc2 gene expression
through epigenetic mechanisms,” concludes the study. “Beyond increase
in basic understanding, our findings have relevance for identifying unique
neurodevelopmental toxicity mechanisms of BPA, which could possibly play a
role in pathogenesis of human neurodevelopmental disorders.”

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