Laboratory of Fear and Anxiety Disorders, Institute of Life Science, Nanchang University, Nanchang, China.
School of Statistics, University of International Business and Economics, Beijing, China.
Brain Behav. 2019 Mar;9(3):e01225. doi: 10.1002/brb3.1225. Epub 2019 Feb 13.
Bisphenol A (BPA) is an endocrine disruptor widely used to manufacture consumer goods. Although the thyroid hormone (TH) disrupting potential of BPA has been thought to be responsible for the neuropsychiatric deficits in the animals that experienced perinatal BPA exposure, the TH availability change at the level of specific brain structures has not been subject to systematic investigation.
In the present study the impacts of perinatal BPA exposure (0.1 mg/L in drinking water) spanning gestation and lactation on TH homeostasis in the prefrontal cortex (PFC) and hippocampus were assessed in male Sprague-Dawley rats at postnatal day 21 (PND21) and PND90. As TH regulates brain glucose metabolism at multiple levels，the effects of BPA treatment on glucose metabolism in the brain tissues were also assessed in adult rats.
The results showed heterogeneous changes in TH concentration induced by BPA between serum and brain tissues, additionally, in the BPA-treated pups, up-regulated expression of the TH transporter monocarboxylate 8 mRNA at PND21 and increased type 3 iodothyronine deiodinase mRNA expressions at PND21 and PND90 were observed. Meanwhile, decreased glucose metabolism was seen in the PFC and hippocampus, while deficits in locomotor activity, spatial memory and social behaviors occurred in BPA-treated groups.
These data support the concept that the developing brain possesses potent mechanisms to compensate for a small reduction in serum TH, such as serum hypothyrodism induced by BPA exposure, however, the long-term negative effect of BPA treatment on TH homeostasis and glucose metabolism may be attributable to neuropsychiatric deficits after mature.
双酚 A（BPA）是一种广泛用于制造消费品的内分泌干扰物。虽然 BPA 具有破坏甲状腺激素（TH）的潜力，被认为是导致经历围产期 BPA 暴露的动物出现神经精神缺陷的原因，但特定脑结构中 TH 可用性的变化尚未受到系统研究。
本研究在雄性 Sprague-Dawley 大鼠中评估了围产期 BPA 暴露（饮用水中 0.1mg/L）对新生后第 21 天（PND21）和第 90 天（PND90）前额叶皮层（PFC）和海马体中 TH 动态平衡的影响。由于 TH 可在多个水平调节大脑葡萄糖代谢，因此还评估了 BPA 处理对成年大鼠脑组织中葡萄糖代谢的影响。
结果表明，BPA 引起的血清和脑组织中 TH 浓度呈异质性变化，此外，在 BPA 处理的幼鼠中，PND21 时 TH 转运体单羧酸转运蛋白 8 mRNA 表达上调，PND21 和 PND90 时 3 型甲状腺素脱碘酶 mRNA 表达增加。同时，PFC 和海马体中的葡萄糖代谢减少，而在 BPA 处理组中出现了运动活动、空间记忆和社会行为缺陷。
这些数据支持这样一种概念，即发育中的大脑具有强大的机制来补偿血清 TH 的少量减少，例如 BPA 暴露引起的血清甲状腺功能减退，但 BPA 处理对 TH 动态平衡和葡萄糖代谢的长期负面影响可能归因于成熟后的神经精神缺陷。
