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Published on: March 6, 2018
Effects of perinatal exposure to bisphenol A on brain neurotransmitters in female rat offspring
Takeshi Honma1, Muneyuki Miyagawa, Megumi Suda
1Department of Health Effects Research, National Institute of Industrial Health, Nagao 6-21-1, Tama-ku, Kawasaki 214-8585, Japan.
Insights
Bisphenol A (BPA) exposure during pregnancy altered brain neurotransmitters in dams and offspring. BPA increased dopamine and serotonin metabolites, and choline levels, suggesting potential neurodevelopmental impacts.
Area of Science:
- Neuroscience
- Toxicology
- Endocrinology
Background:
- Bisphenol A (BPA) is an endocrine-disrupting chemical with weak estrogenic activity.
- Prenatal exposure to environmental chemicals can impact neurodevelopment.
- Understanding BPA's neurochemical effects is crucial for public health.
Purpose of the Study:
- To investigate the effects of prenatal Bisphenol A (BPA) exposure on neurotransmitter levels in pregnant rats and their female offspring.
- To assess dose-dependent neurochemical alterations in the brain.
Main Methods:
- Pregnant Sprague-Dawley rats were administered BPA (4, 40, 400 mg/kg) from gestation day 6 to postnatal day 20.
- Neurotransmitters (dopamine, serotonin) and their metabolites (DOPAC, HVA, 5HIAA) were measured using liquid chromatography.
- Choline and acetylcholine levels were also assessed in brain tissue.
Main Results:
- BPA exposure, particularly at 400 mg/kg, led to maternal toxicity.
- In offspring, increased levels of dopamine and serotonin metabolites were observed at 3 weeks post-birth.
- Elevated choline levels were noted in offspring brains at 6 weeks, and accelerated neurotransmitter turnover occurred in both offspring and dams.
Conclusions:
- Prenatal BPA exposure significantly alters cerebral neurotransmitter systems in dams and female offspring.
- Observed neurochemical changes may be linked to BPA's estrogenic activity, warranting further investigation.
- These findings highlight potential neurodevelopmental risks associated with BPA exposure.
Abstract:
Pregnant Sprague-Dawley (CD IGS) rats were orally administered doses of bisphenol A (BPA) at 4, 40, and 400 mg/kg, from gestation days 6 to postnatal day 20. Neurotransmitters such as dopamine (DA) and serotonin (5HT) were extracted from the brains of dams and female offspring, and measured using liquid chromatography. BPA at 400 mg/kg was toxic and dosed rats died. At 3 wk after birth, brain levels of 3,4-dihydroxyphenylacetic acid (DOPAC, a DA metabolite), homovanillic acid (HVA, a DA metabolite), 5HT, 5-hydroxyindoleacetic acid (5HIAA, a 5HT metabolite) in female offspring were increased and the HVA/DA ratio was high in some brain areas of BPA-treated groups as compared with controls. At the age of 6 wk, levels of choline (Ch) in BPA-treated groups at 4 and 40 mg/kg were higher than control in all of eight brain areas. No changes were observed in acetylcholine (ACh) contents. In 9-wk-old offspring, changes in monoamines and metabolites were scattered and not great. At 3 wk after delivery, levels of 5HIAA in some brain areas of dams treated with BPA were higher than in control dams. Dose dependent increases in HVA and the HVA/DA ratio of the occipital cortex, and in the HVA/DA ratio of the frontal cortex were observed. The turnover of DA and 5HT was accelerated in 3-wk-old offspring and dams. BPA possesses very weak estrogenic activity. Changes in cerebral neurotransmitters observed in offspring and dams in this study may have been related to the estrogenic activity of BPA. However, further investigation is needed to examine the contribution of hormonal activity to such neurotransmitter changes.
