A study suggests that zebrafish, fetal exposure to bisphenol A (BPA), or some non-bisphenol A (BPA) A related chemical products for use in brain development and behavior likely to produce measurable effects. Growing body of literature on the fetal bisphenol A (BPA) exposure of contact problems such as hyperactivity and aggressive behavior in childhood, such as with bisphenol A (BPA) is an endocrine disruptor found in many household products.
Deborah M. Kurrasch and colleagues explored the bisphenol A (BPA) exposure to effects on zebrafish embryos, which constitutes a mechanism to explain the basis of this correlation. This study reveals a low dose of bisphenol A (BPA) – human acceptable daily exposure of 1/1000 – Treatment of zebrafish embryos resulted in the formation of increased hypothalamic original 180% the hypothalamus is a highly conserved region of the brain, involved in the offensive and hyperactivity.
The authors report that exposure to bisphenol S (BPS) which some non-bisphenol A (BPA) commonly used in analog products, has led to increased hypothalamic neurogenesis 240% original. Further studies revealed the formation of a special window at the nerve limited period of bisphenol A (BPA) / bisphenol S (BPS) exposure and hyperactive behavior associated juvenile zebrafish.
The study found that bisphenol A (BPA) and the regulation of neurogenesis associated behavior depends on the androgen receptor activation and upregulation of aromatase. According to the authors, these findings suggest that the use of bisphenol S (BPS) products may not necessarily safer than products containing bisphenol A (BPA) in. Related results are published in the “American Academy of Sciences” on.
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