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

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

Bisphenol-A Neurotoxic Effects on Basal Forebrain Cholinergic Neurons In Vitro and In Vivo

“…To our knowledge, no previous studies have determined the BPA histological effects on BF. Previous studies described neurodegeneration in rat hippocampal and cortical neurons after BPA repeated oral exposure during adulthood [ 49 , 50 , 51 ]. Additionally, single BPA (1 mg/kg) intraperitoneal treatment was shown to induce cellular inflammation, edema, and necrosis in adult rat hippocampal neurons [ 52 ].…”

Effect of bisphenol A on the neurological system: a review update

“…BPA induced apoptotic and necrotic effects in the CA3 neurons of the hippocampus and a significant decrease in hippocampal concentrations of DA, norepinephrine (NE), 5-HT and Ach, as well as in hippocampal AChE activity in rats pre-exposed with EGCG for 2 h before BPA. Abnormal pyramidal cells in the hippocampus and increased hippocampal Casp-3 activity were also demonstrated (El Tabaa et al 2022 ). In another study, in male Wistar albino rats, Caglayan et al .…”

Phytotoxic Effects of Bisphenol a on Growth Indicants And Chlorophyll Content of Pisum Sativum L.

“…Globally, 3700000 tons of BPA is produced every year (Mihaich et al 2009 ). Since, BPA leaches from plastic materials and bottles, human beings come into its contact by eating food and drinks stored in these bottles, cans and packs (Huang et al 2012) and hence it jeopardize the healthiness of humans (Le et al 2008, Wagner and Oehlmann 2009, Cooper et al 2011, Tabaa et al 2022. Humans risk themselves by consuming fish obtained from BPA polluted marine waters (Mita et al 2011).…”

“…Plants could get affected by BPA polluted soils (Pop et al 2021, Yamamoto et al 2001, Zaborowska et al 2021. Few studies are available on the impact of BPA on land plants (Terouchi et al 2004, Ferrara et al 2006) in relation to the impact of BPA on animals (Flint et al 2012, Tabaa et al 2022. There is limited documented work available on the toxicologic effect of BPA on plants which take in and accumulate it from BPA polluted agricultural soils (Ferrara et al 2006).…”