Does (\u2009\u2212)-epigallocatechin-3-gallate protect the neurotoxicity induced by bisphenol A in vivo?

Manar Mohammed El Tabaa,Inas Zakria Abd El Salam,Samia Salem Sokkar,Ehab Sayed Ramdan,Anis Anis

doi:10.1007/s11356-021-18408-z

Manar Mohammed El Tabaa, Inas Zakria Abd El Salam + Show 3 more

Open Access

https://doi.org/10.1007/s11356-021-18408-z

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Abstract

Bisphenol A (BPA) is one of the chemicals that is firmly accompanied by hippocampal neuronal injury. As oxidative stress appears to be a major contributor to neurotoxicity induced by BPA, antioxidants with remarkable neuroprotective effects can play a valuable protective role. Around the world, ( −)-epigallocatechin-3-gallate (EGCG) was one of the most popular antioxidants that could exert a beneficial neuroprotective role. Here, we examined the potential efficiency of EGCG against neurotoxicity induced by BPA in the hippocampal CA3 region of the rat model. This study revealed that EGCG was unable to abrogate the significant decrease in circulating adiponectin level and hippocampal superoxide dismutase activity as well as an increase in hippocampal levels of nitric oxide and malondialdehyde. Notably, EGCG failed to antagonize the oxidative inhibitory effect of BPA on hippocampal neurotransmission and its associated cognitive deficits. In addition, the histopathological examination with immunohistochemical detection of caspase-3 and NF-kB/p65 emphasized that EGCG failed to protect hippocampal CA3 neurons from apoptotic and necrotic effects induced by BPA. Our study revealed that EGCG showed no protective role against the neurotoxic effect caused by BPA, which may be attributed to its failure to counteract the BPA-induced oxidative stress in vivo. The controversial effect is probably related to EGCG’s ability to impede BPA glucuronidation and thus, its detoxification. That inference requires further additional experimental and clinical studies.Graphical abstract

Highlights

Bisphenol A (BPA; 4, 40-isopropylidenediphenol) is a widely used synthetic substance that has been found in a variety of everyday consumer items, including polycarbonate plastics and epoxy resins (Li and Suh 2019)
Bisphenol A (BPA) is a dangerous environmental contaminant that has been implicated in the development of neurotoxicity (Santoro et al 2019)
Various lines of evidence show that BPA can cause oxidative stress in the hippocampus, interfering with the synthesis and release of several central neurotransmitters as a result (Rebolledo-Solleiro et al 2021)

Summary

Introduction

Bisphenol A (BPA; 4, 40-isopropylidenediphenol) is a widely used synthetic substance that has been found in a variety of everyday consumer items, including polycarbonate plastics and epoxy resins (Li and Suh 2019). Because BPA is continuously released around the world, it can infiltrate the environment and find its way into our bodies, causing a variety of negative health effects such as reproductive and developmental toxicity, metabolic disorders, immunotoxicity, neurobehavioral effects, and neurotoxicity (Bilal et al 2019 and Li and Suh 2019). Given that BPA exposure through food is the most dangerous of all the ways (Almeida et al 2018), regulatory organizations such as the United States Environmental Protection Agency (USEPA) had to establish a reference safe dosage (RfD) for chronic oral BPA intake, which was. The neurotoxic effect of BPA is supposed to arise from its antiestrogenic properties and accompanying overproduction of reactive oxygen and nitrogen species (ROS/RNS) (Chen et al 2017), which was detected to inversely correlated with the serum adiponectin level (Li and Shen 2019). Through a mechanism involving the activation of the adenosine monophosphate-activated protein kinase (AMPK) signaling pathway, adiponectin was found to have a neuroprotective impact by decreasing ROS production and increasing eNOS activity (Rashtiani et al 2021)

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