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

Abstract

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.

Protective effect of polysaccharides isolated from Sargassum horneri against H 2 O 2 -induced oxidative stress in vitro in Vero and in vivo in zebrafish

“…Several studies have shown that oxidative stress can reduce zebra sh survival and lead to malformation (Chowdhury and Saikia, 2022;Gyimah et al, 2022;Hahn et al, 2015). In combination with the zebra sh survival rate and growth and development, we selected 7 mmol L − 1 of H 2 O 2 to induce zebra sh.…”

Neurodevelopmental toxicity of bisphenol AF in zebrafish larvae and the protective effects of curcumin

“…Similarly, exposure to BPA and bisphenol analogs has been reported to affect neurotransmission; for example, AChE activity was clearly decreased in the hippocampus of mice with BPA (Luo et al, 2013) and in Daphnia magna with BPF (Liu et al, 2020). Besides, BPAF was also reported to inhibit dopaminergic signaling and metabolism of neurotransmitters in zebrafish (Gu et al, 2022; Gyimah et al, 2022). Consistent with the former result, CUR could significantly rescue the decreased AChE activity caused by BPAF.…”

Isavuconazole induces neurodevelopment defects and motor behaviour impairment in zebrafish embryos

“…Studies have found that under normal physiological conditions, sh and other vertebrates can rapidly clear ROS through antioxidant enzymes, such as superoxide dismutase and catalase [24]. However, some high-dose clinical drugs can cause excessive generation of reactive oxygen species (ROS) in tissues, thereby destroying major cellular macromolecules and inducing oxidative stress leading to cell damage and apoptosis [25][26].…”