Bisphenol F exposure impairs neurodevelopment in zebrafish larvae (Danio rerio)

Gu, Jie; Wu, Jiang; Xu, Shuqin; Zhang, Liye; Fan, Deling; Shi, Lili; Wang, Jun; Ji, Guixiang

doi:10.1016/j.ecoenv.2019.109870

Cited by 62 publications

(34 citation statements)

References 32 publications

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“…Similar to these ndings, Maćczak et al found decreased levels of CAT in human erythrocytes treated with BPF for different periods of time (4 h and 24 h) [15]. Decreased CAT activity was also found in juvenile common carp [37], and the larvae of zebra sh after waterborne exposure to BPF [7]. Ullah et al, also reported that CAT activity was inhibited in the testicular tissues of rats exposed to BPF via drinking water [5].…”

Section: Discussionmentioning

confidence: 55%

“…It has been reported that BPF enhances ROS levels and leads to increased levels of lipid peroxidation in human erythrocytes [15]. In another study, BPF resulted in a high level of MDA contents and nally led to apoptosis in the larvae of zebra sh [7]. Ullah et al [5] also reported increased levels of lipid peroxidation and ROS in the reproductive tissues of male rats after exposure to BPF.…”

Section: Discussionmentioning

confidence: 94%

“…On the other hand, no signi cant changes were seen in the SOD activity of juvenile common carp liver (Cyprinus carpio) samples after long-term (60 days) waterborne exposure to BPF [38]. Conversely, Gu et al [7] stated decreased SOD activities in the larvae of zebra sh treated with BPF concentrations of 7-700 µg/L for 3 and 6 days. It can be said that the different ndings regarding the SOD activities as a consequence of BPF exposure might have depended on the applied BPF concentration, and design and duration of the experiment.…”

Section: Discussionmentioning

confidence: 97%

“…Recent studies have reported that BPA analogues, including BPF, have caused developmental abnormalities in the reproductive tissues of male rats, altering their hormonal balance and antioxidant defences [5]. Similar to BPA, the genotoxic, immunotoxic, and neurotoxic potentials of its analogues have been reported in some experimental studies over last decade [6][7][8].…”

Section: Introductionmentioning

confidence: 98%

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In vitro effects of bisphenol F on antioxidant system indicators in the isolated hepatocytes of rainbow trout (Oncorhyncus mykiss)

Aykut

Kaptaner

2021

Mol Biol Rep

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Bisphenol F (BPF) has been used frequently in the plastics industry and the production of daily consumer products as an alternative to bisphenol A (BPA). It was aimed herein to determine the cytotoxic effects of BPF on hepatocytes isolated from the liver of rainbow trout (Oncorhyncus mykiss) using lactate dehydrogenase (LDH) assay and antioxidant defence system indicators. The cultured hepatocytes were exposed to seven concentrations (0, 15.63, 31.25, 62.50, 125, 250, and 500 µM) of BPF for 24 h. According to the LDH assay, the percentage of cytotoxicity was increased dose dependently in the cells.The malondialdehyde content, which is indicative of lipid peroxidation, was increased signi cantly at BPF concentrations between 15.63 and 250 µM, whereas it remained unchanged with a concentration of 500 µM. The activities of superoxide dismutase were increased, while those of catalase were decreased with all of the BPF concentrations. Elevated levels of reduced glutathione content were determined with BPF concentrations between 15.63 and 250 µM, but decreased signi cantly with a concentration of 500 µM.Signi cant increases in the activities of the glutathione peroxidase were found in hepatocytes treated with BPF at concentrations of 31.25 to 500 µM. GST activity was only signi cantly increased with a BPF concentration of 250 µM. The results showed that the toxic mechanism of BPF was mainly based on cell membrane damage and oxidative stress, which have an in uence on antioxidant defences. Therefore, BPF was reconsidered as a safe alternative instead of BPA in the manufacturing of industrial or daily products.

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Section: Discussionmentioning

confidence: 55%

Section: Discussionmentioning

confidence: 94%

Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 98%

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In vitro effects of bisphenol F on antioxidant system indicators in the isolated hepatocytes of rainbow trout (Oncorhyncus mykiss)

Aykut

Kaptaner

2021

Mol Biol Rep

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“…Other studies have shown that PCBs increase cell death in in vitro primary hippocampal but not cortical cultures (Howard, Fitzpatrick, Pessah, Kostyniak, & Lein, 2003). For bisphenols, exposure of larvae to bisphenol F increased apoptosis in the whole brain (Gu et al, 2020), and Xenopus laevis embryos exposed to BPA had increased brain apoptosis (Oka et al, 2003). As a whole, this literature suggests a loss of certain neural populations due to embryonic exposure to EDCs.…”

Section: Pcbs Can Disrupt the Balance Of Neural Cell Birth And Deathmentioning

confidence: 84%

Exposure to prenatal PCBs shifts the timing of neurogenesis in the hypothalamus of developing rats

2020

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The developing brain is highly sensitive to the hormonal milieu, with gonadal steroid hormones involved in neurogenesis, neural survival, and brain organization. Limited available evidence suggests that endocrine‐disrupting chemicals (EDCs) may perturb these developmental processes. In this study, we tested the hypothesis that prenatal exposure to a mixture of polychlorinated biphenyls (PCBs), Aroclor 1221, would disrupt the normal timing of neurogenesis in two hypothalamic regions: the ventromedial nucleus (VMN) and the preoptic area (POA). These regions were selected because of their important roles in the control of sociosexual behaviors that are perturbed in adulthood by prenatal EDC exposure. Pregnant Sprague–Dawley rats were exposed to PCBs from Embryonic Day 8 (E8) to E18, encompassing the period of neurogenesis of all hypothalamic neurons. To determine the birth dates of neurons, bromo‐2‐deoxy‐5‐uridine (BrdU) was administered to dams on E12, E14, or E16. On the day after birth, male and female pups were perfused, brains immunolabeled for BrdU, and numbers of cells counted. In the VMN, exposure to PCBs significantly advanced the timing of neurogenesis compared to vehicle‐treated pups, without changing the total number of BrdU+ cells. In the POA, PCBs did not change the timing of neurogenesis nor the total number of cells born. This is the first study to show that PCBs can shift the timing of neurogenesis in the hypothalamus, specifically in the VMN but not the POA. This result has implications for functions controlled by the VMN, especially sociosexual behaviors, as well as for sexual selection more generally.

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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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Bisphenol F exposure impairs neurodevelopment in zebrafish larvae (Danio rerio)

Cited by 62 publications

References 32 publications

In vitro effects of bisphenol F on antioxidant system indicators in the isolated hepatocytes of rainbow trout (Oncorhyncus mykiss)

In vitro effects of bisphenol F on antioxidant system indicators in the isolated hepatocytes of rainbow trout (Oncorhyncus mykiss)

Exposure to prenatal PCBs shifts the timing of neurogenesis in the hypothalamus of developing rats

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

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