Bisphenol AF (BPAF) is a structural counterpart of bisphenol A (BPA) that is utilized in the food and beverage industry. The present study has 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 hpf. Locomotor activity of the larvae (at 120 hpf) significantly decreased from dark-light, but increased from light-dark transitions, in BPAF groups (0.1 μM, 0.3 μM and 1.0 μM). Acridine orange result showed that BPAF significantly increased green fluorescence protein intensity (22.6%) in the 1.0 μM group. Consistently, the induced apoptosis significantly upregulated caspase 3 in 0.3 μM (1.95 fold) and 1.0 μM (2.26 fold); and bax in folds of 1.60- and 1.78 in 0.3 μM and 1.0 μM, respectively; while bcl-2 expression was significantly decreased in 0.3 μM (0.72-fold) and 1.0 μM (0.53-fold). Additionally, increased ROS concentrations in 0.3 μM (27%) and 1.0 μM (61.4%) resulted in suppressed SOD and CAT activities. Moreover, qPCR results depicted that BPAF (0.3 μM and 1.0 μM) significantly altered the normal dopaminergic signalling where dat was upregulated, while drd2a and th1 were downregulated, 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 early indicator to BPAF exposure. This article is protected by copyright. All rights reserved. © 2022 SETAC.