The effects of perinatal bisphenol A exposure on thyroid hormone homeostasis and glucose metabolism in the prefrontal cortex and hippocampus of rats.

Xiaobin Xu,Yuanqiao Guo,Wenhua Zhang,Bing‐Xing Pan,Ruei Tan,Junyu Zhang,Nobumasa Kato,Shijun Fan

doi:10.1002/brb3.1225

Xiaobin Xu, Yuanqiao Guo + Show 6 more

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https://doi.org/10.1002/brb3.1225

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Abstract

IntroductionBisphenol 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.MethodsIn 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.ResultsThe 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.ConclusionThese 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.

Highlights

Bisphenol A (BPA) is an endocrine disruptor widely used to manufac‐ ture consumer goods
Our previous study has demonstrated that perinatal constant BPA exposure at a low dose of 0.1 mg/L via maternal drinking water, which is equivalent to about 15 μg kg‐1 day‐1 BPA intake (Xu et al, 2012), induced a mean BPA level of 1.7 ng/ml in serum in 21‐ day‐old pup rats which is lower than the mean value observed in girls and boys (Chen et al, 2015; Komarowska et al, 2015), and caused hyperactivity, impaired spatial memory and deficit of con‐ textual fear learning in adulthood (Xu et al, 2014, 2017)
The mechanisms underlying the actions of BPA on the development of brain are not well understood, one hypothesis was advanced that affected thyroid hormone (TH) homeostasis may be involved in the adverse consequences of BPA exposure, because of the change in serum TH level in newborns perinatally exposed to BPA (Birnbaum et al, 2012; Xu et al, 2007; Zoeller, Bansal, & Parris, 2005) and profound actions of TH on brain development and func‐ tion (Ahmed, El‐Gareib, El‐Bakry, Abd El‐Tawab, & Ahmed, 2008)

Summary

Introduction

Bisphenol A (BPA) is an endocrine disruptor widely used to manufac‐ ture consumer goods. The fresh tissue (25 mg) was quickly into 30 mmol/L sodium phosphate buffer (pH 7.0) and homogenized in ice bath; after centrifugation at 10,000 g for 5 min at 4°C, 5 μl of supernatant was added to a 96‐well plate and the volume was adjusted to 50 μl with AChE assay buffer; 50 μl of reaction mix was added to each well containing choline standards, positive control and samples; after incubation for 30 min at 37°C, the absorbance at

Results

Conclusion