Perinatal low-dose bisphenol AF exposure impairs synaptic plasticity and cognitive function of adult offspring in a sex-dependent manner

Zhang, Chao; Wu, Xiaochang; Li, Sha; Dou, Lianjie; Zhou, Li; Wang, Feng-hui; Ma, Kai; Huang, Dan; Pan, Ying; Gu, Jijun; Cao, Jiyu; Wang, Hua; Hao, Jiahu

doi:10.1016/j.scitotenv.2021.147918

Cited by 21 publications

(2 citation statements)

References 80 publications

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“…A recent study has reported that 200 μg/L BPA/BPAF remarkably reduced the locomotor activity of zebrafish larvae (Gu et al, 2022). In addition, in vitro and in vivo studies have indicated the neurotoxic potency of BPAF using a hippocampal cell line (HT‐22; Lee et al, 2013) and a mouse model (Zhang et al, 2021). In particular, studies on environmental neurotoxicity of BPAF in zebrafish are limited by insufficient data regarding exposures in early embryonic developmental stages.…”

Section: Introductionmentioning

confidence: 99%

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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Section: Introductionmentioning

confidence: 99%

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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“…Apart from metal toxicants, endocrine-disrupting chemicals (EDCs) such as bisphenol-A also impacts the behaviors of offspring [ 114 ]. The expression of hippocampal PSD-95 and Synapsin-1 are significantly downregulated after exposure to BPA perinatally, but only in male offspring [ 104 ]. This sex-specific manner may be associated with differential methylation pattern in ERα promoters of different sexes.…”

Section: Multisystem Diseasesmentioning

confidence: 99%

Developmental origins of adult diseases

Liu

Huang

et al. 2022

Medical Review

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The occurrence and mechanisms of developmental adult diseases have gradually attracted attention in recent years. Exposure of gametes and embryos to adverse environments, especially during plastic development, can alter the expression of certain tissue-specific genes, leading to increased susceptibility to certain diseases in adulthood, such as diabetes, cardiovascular disease, neuropsychiatric, and reproductive system diseases, etc. The occurrence of chronic disease in adulthood is partly due to genetic factors, and the remaining risk is partly due to environmental-dependent epigenetic information alteration, including DNA methylation, histone modifications, and noncoding RNAs. Changes in this epigenetic information potentially damage our health, which has also been supported by numerous epidemiological and animal studies in recent years. Environmental factors functionally affect embryo development through epimutation, transmitting diseases to offspring and even later generations. This review mainly elaborated on the concept of developmental origins of adult diseases, and revealed the epigenetic mechanisms underlying these events, discussed the theoretical basis for the prevention and treatment of related diseases.

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Bisphenol AF induces multiple behavioral and biochemical changes in zebrafish (Danio rerio) at different life stages

Rao

Cao

et al. 2022

Aquatic Toxicology

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Perinatal low-dose bisphenol AF exposure impairs synaptic plasticity and cognitive function of adult offspring in a sex-dependent manner

Cited by 21 publications

References 80 publications

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

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

Developmental origins of adult diseases

Bisphenol AF induces multiple behavioral and biochemical changes in zebrafish (Danio rerio) at different life stages

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