Impact of BPA on behavior, neurodevelopment and neurodegeneration Daniela

Rebolledo-Solleiro, Daniela; Flores, Laura; Solleiro-Villavicencio, Helena

doi:10.2741/4898

Cited by 44 publications

(17 citation statements)

References 24 publications

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“…Everyone has been forced to be exposed to the neurotoxic impact of BPA as a result of uncontrolled expansion in the manufacture and usage of BPA-containing commercial items (Mg et al 2022). 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). Jointly, antioxidants have received increased attention for their potential involvement in alleviating BPA-induced damage (Amjad et al 2020).…”

Section: Discussionmentioning

confidence: 99%

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

Tabaa

Sokkar

Ramdan

et al. 2022

Environ Sci Pollut Res

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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

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Section: Discussionmentioning

confidence: 99%

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

Tabaa

Sokkar

Ramdan

et al. 2022

Environ Sci Pollut Res

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“…Although the exact neurodegenerative effect of BPA on the neuronal structures supplying the urinary bladder has not yet been confirmed, previous observations indicating BPA-induced urinary voiding disruption 20 , strongly suggest that such phenomenon may also be observed in this organ, similar to other parts of the nervous system 65 , 66 . Thus, considering the neurotoxic effects of BPA and VIP’s role as a key neuroprotective factor for autonomic neurons, the observed fluctuations in the expression pattern of VIP—were most probably of a compensatory nature.…”

Section: Discussionmentioning

confidence: 94%

Bisphenol A affects vipergic nervous structures in the porcine urinary bladder trigone

Makowska

Lech²,

Majewski

et al. 2021

Sci Rep

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Bisphenol A (BPA) is used in the production of plastics approved for contact with feed and food. Upon entering living organisms, BPA, as a potent endocrine disruptor, negatively affects various internal organs and regulatory systems, especially in young individuals. Although previous studies have described the neurotoxic effects of BPA on various tissues, it should be underlined that the putative influence of this substance on the chemical architecture of the urinary bladder intrinsic innervation has not yet been studied. One of the most important neuronal substances involved in the regulation of urinary bladder functions is vasoactive intestinal polypeptide (VIP), which primarily participates in the regulation of muscular activity and blood flow. Therefore, this study aimed to determine the influence of various doses of BPA on the distribution pattern of VIP-positive neural structures located in the wall of the porcine urinary bladder trigone using the double-immunofluorescence method. The obtained results show that BPA influence leads to an increase in the number of both neurons and nerve fibres containing VIP in the porcine urinary bladder trigone. This may indicate that VIP participates in adaptive processes of the urinary bladder evoked by BPA.

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“…Of the groups that identified BPA-associated anxiety-like behavior, Kumar et al found perinatal exposure to BPA alters the ratio of excitatory to inhibitory synaptic densities [109]. Imbalances in neural excitation and inhibition have been reported in the pathophysiology of many Several recent reviews have also discussed neurobehavioral ramifications of BPA exposure in animal models [146][147][148][149][150]. Although not reviewed here, many other behaviors have been associated with early BPA exposure, including visual perception [101,128], depression-like behavior [141,151], and social and reproductive behaviors [142,147,152].…”

Section: Behavior Is Impacted By Bpamentioning

confidence: 99%

Does Bisphenol A Confer Risk of Neurodevelopmental Disorders? What We’ve Learned from Developmental Neurotoxicity Studies in Animal Models

Welch¹,

Mulligan²

2022

Preprint

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Substantial evidence indicates that bisphenol A (BPA), a ubiquitous environmental chemical used in the synthesis of polycarbonate plastics and epoxy resins, can impair brain development. Clinical and epidemiological studies exploring potential connections between BPA and neurodevelopmental disorders in humans have repeatedly identified correlations between early BPA exposure and developmental disorders, like attention deficit/hyperactivity disorder and autism spectrum disorder. Investigations using invertebrate and vertebrate animal models have revealed that developmental exposure to BPA can impair multiple aspects of neuronal development, including neural stem cell proliferation and differentiation, synapse formation, and synaptic plasticity—neuronal phenotypes that are thought to underpin the fundamental changes in behavior associated neurodevelopmental disorders. Consistent with BPA-associated neuronal phenotypes, behavioral analyses of BPA-treated animals have shown significant impacts on behavioral endophenotypes related to neurodevelopmental disorders, including altered locomotor activity, learning and memory deficits, and anxiety-like behavior. To contextualize the correlations between BPA and neurodevelopmental disorders in humans, this review summarizes current literature reporting on the developmental neurotoxicity of BPA in laboratory animals, with an emphasis on neuronal phenotypes, molecular mechanisms, and behavioral outcomes. The collective works described here predominantly support the notion that gestational exposure to BPA should be regarded as a risk factor for neurodevelopmental disorders.

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Impact of BPA on behavior, neurodevelopment and neurodegeneration Daniela

Cited by 44 publications

References 24 publications

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

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

Bisphenol A affects vipergic nervous structures in the porcine urinary bladder trigone

Does Bisphenol A Confer Risk of Neurodevelopmental Disorders? What We’ve Learned from Developmental Neurotoxicity Studies in Animal Models

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