Bisphenol A (BPA), a chemical that is widely used in the manufacture of polycarbonate polymers, epoxy resins and other plastic materials, poses a threat in the development of central nervous system, says a study at Duke Medicine, according to Medical Xpress.
Researchers at Duke Medicine conducted a series of experiments to discover how exposure to BPA interferes with the development of the central nervous system in humans and animals. Over the years there have been concerns over BPA's effect in brain development but the causes of this occurrence were not understood completely.
"Our study found that BPA may impair the development of the central nervous system, and raises the question as to whether exposure could predispose animals and humans to neurodevelopmental disorders," said lead author Wolfgang Liedtke, M.D., PhD, associate professor of medicine/neurology and neurobiology at Duke, according to the report.
Several studies conducted on animals show evidence of BPA having negative health effects including obesity, reproductive and neurological disorders, cancer and immune system disorders. Noting the risk factors, United States Food and Drug Administration cautioned about the vulnerabilities to foetuses, infants, and young children and banned the use of chemical in the manufacture of baby bottles and cups in July 2012.
High levels of chloride are present in the cells of maturing neurons, which eventually drop as they mature. This important step is carried out by a protein called KCC2, which removes the chloride ions out of the cells.
The negative reaction initiates when these chloride ions are not removed from the cells by the KCC2, resulting in the interruption of developing nervous system.
During the research, when a small quantity of BPA was introduced in the neurons, Kcc2 gene was suppressed by the chloride ions making it difficult for the KCC2 protein to remove the chloride from the neurons.
Researchers found the main cause of the Kcc2 gene shutting down. A protein that helps in the normal functioning of the brain, named MECP2 attaches to the Kcc2 gene at a higher rate when exposed to BPA and it prevents the Kcc2 gene from responding.
"Our findings improve our understanding of how environmental exposure to BPA can affect the regulation of the Kcc2 gene. However, we expect future studies to focus on what targets aside from Kcc2 are affected by BPA," Liedtke said. "This is a chapter in an ongoing story."
The findings also noted that female neurons were at a higher risk as the chloride shift is more severe in female neurons than male neurons when exposed to BPA.
Further research will shed more light on the sex-specific effects of BPA exposure, researchers say.
The findings of the study are published in an online journal, Proceedings of the National Academy of Sciences.
