Study reveals that prenatal exposure to BPA disrupts aromatase activity in male brains, potentially leading to autism-like symptoms. Treatment with 10-HDA shows promise in reversing these effects.
By Dr. Chinta SidharthanReviewed by Benedette Cuffari, M.Sc.Aug 11 2024 In a recent study published in Nature Communications, researchers investigated the role of aromatase in the increased risk of autism spectrum disorder observed in males prenatally exposed to bisphenol A .
Aromatase is an enzyme encoded by the CYP19A1 gene that is expressed and regulated in the brain. Aromatase converts androgens to estrogens and is found in high levels in the amygdala of males during fetal development. Post-mortem analyses of males with autism have observed lower levels of aromatase activity than in the brains of age-matched healthy controls. A 38% reduction of CYP19A1 expression in the prefrontal cortex of males with autism was also observed.
The researchers also proposed that estrogen supplementation in the form of 10-hydroxy-2-decenoic acid , which is commonly found in royal jelly from beehives, could ameliorate the impact of prenatal BPA exposure and improve ASD phenotypes in a murine model. In vitro experiments using the human neuroblastoma cell line SH-SY5Y demonstrated that BPA exposure reduces aromatase expression levels by 50%. Compared to control mice, prenatal BPA exposure similarly reduced the expression of aromatase in the brains of male mice.
Prenatal Amygdala Brain Children DNA DNA Methylation Enzyme Estrogen Gene In Utero In Vitro In Vivo Phenotype Research Spine
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