Developmental neurotoxicity of low concentrations of bisphenol A and S exposure in zebrafish

Gyimah, Eric; Xu, Hai; Dong, Xiyang; Qiu, Xuchun; Zhang, Zhen; Bu, Yuanqing; Akoto, Osei

doi:10.1016/j.chemosphere.2020.128045

Cited by 46 publications

(22 citation statements)

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“…2 , 4 ). Generally, this finding is consistent with the literature; however, the exact level of BPA to elicit these effects varies greatly ( Lam et al, 2011 ; Saili et al, 2012 ; Tse et al, 2013 ; Wang et al, 2013 ; Martínez et al, 2018 ; Olsvik et al, 2019 ; Coumailleau et al, 2020 ; Gyimah et al, 2021 ; Huang et al, 2021 ; Scopel et al, 2021 ; Sundarraj et al, 2021 ; Wu et al, 2021 ). The differences in the reported concentrations of BPA required to elicit deformity and mortality likely result from variation in experimental protocols or the strain of zebrafish used.…”

Section: Discussionsupporting

confidence: 92%

“…The differences in the reported concentrations of BPA required to elicit deformity and mortality likely result from variation in experimental protocols or the strain of zebrafish used. Similar to deformity and mortality, hatching delays have more commonly been reported with higher levels of BPA ( Martínez et al, 2018 ; Scopel et al, 2021 ; but see Olsvik et al, 2019 compared with lower levels of BPA ( Gyimah et al, 2021 ; Huang et al, 2021 ; Gu et al, 2022 ; but see Sundarraj et al, 2021 ). By contrast, very low levels of BPA have been reported to accelerate hatching ( Qiu et al, 2016 ; Coumailleau et al, 2020 ).…”

Section: Discussionmentioning

confidence: 84%

“…Numerous studies have found that BPA affects locomotion in zebrafish. However, there is little consistency in reported behavioral outcomes ( Saili et al, 2012 ; Wang et al, 2013 ; Kinch et al, 2015 ; Fraser et al, 2017 ; Olsvik et al, 2019 ; Coumailleau et al, 2020 ; Gyimah et al, 2021 ; Wu et al, 2021 ). We observed no changes in the total distance moved or in repetitive behavior (circling; Fig.…”

Section: Discussionmentioning

confidence: 99%

“…It has been found that exposure to relatively high concentrations of BPA early in the zebrafish life cycle increases mortality and deformity, and delays hatching. Interestingly, despite general agreement regarding the adverse effects of high levels of BPA on mortality, body shape, and time of hatching, the reported threshold concentration of BPA for producing these effects varies greatly ( Lam et al, 2011 ; Saili et al, 2012 ; Tse et al, 2013 ; Wang et al, 2013 ; Martínez et al, 2018 ; Olsvik et al, 2019 ; Coumailleau et al, 2020 ; Gyimah et al, 2021 ; Huang et al, 2021 ; Scopel et al, 2021 ; Sundarraj et al, 2021 ; Wu et al, 2021 ). Furthermore, some studies have found that BPA exposure modifies locomotion in zebrafish, whereas others have not ( Saili et al, 2012 ; Wang et al, 2013 ; Kinch et al, 2015 ; Fraser et al, 2017 ; Olsvik et al, 2019 ; Coumailleau et al, 2020 ; Gyimah et al, 2021 ; Wu et al, 2021 ).…”

Section: Introductionmentioning

confidence: 99%

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Bisphenol A Exposure Induces Sensory Processing Deficits in Larval Zebrafish during Neurodevelopment

Scaramella

Alzagatiti

Creighton

et al. 2022

eNeuro

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Because of their ex utero development, relatively simple nervous system, translucency, and availability of tools to investigate neural function, larval zebrafish are an exceptional model for understanding neurodevelopmental disorders and the consequences of environmental toxins. Furthermore, early in development, zebrafish larvae easily absorb chemicals from water, a significant advantage over methods required to expose developing organisms to chemical agents in utero . Bisphenol A (BPA) and BPA analogs are ubiquitous environmental toxins with known molecular consequences. All humans have measurable quantities of BPA in their bodies. Most concerning, the level of BPA exposure is correlated with neurodevelopmental difficulties in people. Given the importance of understanding the health-related effects of this common toxin, we have exploited the experimental advantages of the larval zebrafish model system to investigate the behavioral and anatomic effects of BPA exposure. We discovered that BPA exposure early in development leads to deficits in the processing of sensory information, as indicated by BPA’s effects on prepulse inhibition (PPI) and short-term habituation (STH) of the C-start reflex. We observed no changes in locomotion, thigmotaxis, and repetitive behaviors (circling). Despite changes in sensory processing, we detected no regional or whole-brain volume changes. Our results show that early BPA exposure can induce sensory processing deficits, as revealed by alterations in simple behaviors that are mediated by a well-defined neural circuit.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 84%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Bisphenol A Exposure Induces Sensory Processing Deficits in Larval Zebrafish during Neurodevelopment

Scaramella

Alzagatiti

Creighton

et al. 2022

eNeuro

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“…Cependant, le BPA peut se lier à d'autres récepteurs nucléaires ou membranaires (1). Le BPA (et BPS), activant le récepteur aux androgènes, induit l'activation de l'aromatase B, aboutissant à une neurogenèse précoce dans l'hypothalamus et à un comportement hyperactif (67). La neurotoxicité peut également être liée au stress oxydant générant une apoptose et affecter le comportement locomoteur (70).…”

Section: Etudes Expérimentales Modes D'action Et Mécanismesunclassified

Polluants in materials of everyday life and neurodevelopment in children

Etiemble¹,

Cordier²

2022

Environnement Risques Santé

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L'exposition à des polluants présents à faibles concentrations dans les matériaux de la vie quotidienne (retardateurs de flamme, composés perfluorés, bisphénols, phtalates), considérés comme des perturbateurs endocriniens, a été associée à des perturbations du neurodéveloppement chez l'enfant dans des études prospectives. La force de l'association varie selon les substances, les différents congénères et les métabolites. La période prénatale représente la période de vulnérabilité pendant laquelle les substances peuvent altérer la trajectoire développementale du cerveau. Des associations sont mises en évidence dans les études avec des altérations psychomotrices, cognitives et comportementales : principalement dans le domaine cognitif avec les retardateurs de flamme ; dans le domaine comportemental avec les phtalates et les bisphénols. Les effets associés aux expositions sont plus fréquents chez les garçons, les filles sont concernées surtout avec les bisphénols. L'implication de ces substances dans la prévalence des troubles du spectre autistique (TSA) et du trouble déficit d'attention/hyperactivité (TDAH) reste incertaine. Des effets sur le comportement et les capacités d'apprentissage sont décrits dans les études expérimentales. La modification de l'homéostasie des hormones thyroïdiennes est une des hypothèses pouvant expliquer les effets comme perturbateurs endocriniens mais des interactions avec d'autres systèmes hormonaux et de neurotransmission peuvent également perturber les différents processus neurodéveloppementaux selon le sexe. Des modifications épigénétiques de l'expression de gènes essentiels au développement du cerveau sont associées à l'exposition à ces polluants.

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Oxidative Stress and Apoptosis in Bisphenol AF–Induced Neurotoxicity in Zebrafish Embryos

Gyimah

Zhu

Zhang

et al. 2022

Enviro Toxic and Chemistry

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Bisphenol AF (BPAF) is a structural counterpart of bisphenol A that is utilized in the food and beverage industry.The present study investigated the potential mechanisms in BPAF-induced neurotoxicity in zebrafish embryos. The BPAF concentrations (0.03, 0.1, 0.3, and 1.0 µM) had no obvious effect on hatching, mortality, and body length of zebrafish larvae, while curved tail and pericardial edema were observed in the 1.0 μM group at 72 and 96 h postfertilization (hpf). Locomotor activity of the larvae (at 120 hpf) significantly decreased from dark to light but increased from light to dark transitions in BPAF groups (0.1, 0.3, and 1.0 μM). Acridine orange showed that BPAF significantly increased green fluorescence protein intensity (22.6%) in the 1.0 μM group. Consistently, the induced apoptosis significantly up-regulated caspase 3 at 0.3 μM (1.95-fold) and 1.0 μM (2.26-fold) and bax at 0.3 μM (1.60-fold) and 1.0 μM (1.78-fold), whereas bcl-2 expression was significantly decreased at 0.3 μM (0.72-fold) and 1.0 μM (0.53-fold). In addition, increased reactive oxygen species concentrations at 0.3 μM (27%) and 1.0 μM (61.4%) resulted in suppressed superoxide dismutase and catalase activities. Moreover, quantitative polymerase chain reaction results showed that BPAF (0.3 and 1.0 μM) significantly altered normal dopaminergic signaling where dat was up-regulated, while drd2a and th1 were down-regulated, in a concentration-dependent manner. Aberrations in dopamine-related genes were congruous with the dysregulations in neurodevelopment genes (sox11b, pax6a, syn2a, and rob2). Our findings suggest that BPAF-evoked oxidative stress and apoptosis could translate into phenotypical behavioral and neurodevelopmental abnormalities. These highlights could provide theoretical reference for risk assessment and act as an early indicator to BPAF exposure.

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Developmental neurotoxicity of low concentrations of bisphenol A and S exposure in zebrafish

Cited by 46 publications

References 47 publications

Bisphenol A Exposure Induces Sensory Processing Deficits in Larval Zebrafish during Neurodevelopment

Bisphenol A Exposure Induces Sensory Processing Deficits in Larval Zebrafish during Neurodevelopment

Polluants in materials of everyday life and neurodevelopment in children

Oxidative Stress and Apoptosis in Bisphenol AF–Induced Neurotoxicity in Zebrafish Embryos

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