Although Bisphenol F (BPF), a bisphenol A (BPA) analogue with a similar chemical structure to that of BPA, is widely used in commercial products, little is known about its potential toxic effects on the reproductive neuroendocrine system in vivo. The present study aimed to comprehensively evaluate the effects of BPF on the reproductive neuroendocrine system in zebrafish and to assess the potential mechanisms underlying its association with estrogen receptor (ER) and aromatase (AROM) pathways. Long-term exposure to environmentally relevant and low levels of BPF led to increased expression of reproductive neuroendocrine-related genes (kiss1, kiss1r, gnrh3, lhβ, and fshβ) in the zebrafish brain, as well as increased levels of adrenocorticotropic, gonadotropin-releasing, luteinizing, and follicle-stimulating hormones in the zebrafish brain and vitellogenin in the zebrafish liver. In addition, these effects were associated with an increase in erα, erβ, cyp19a, and cyp19b activity. Meanwhile, ER and AROM antagonists, alone or in combination, significantly attenuated the stimulation of kiss1, lhβ, vtg, and gnrh3 expression, thereby suggesting that chronic BPF exposure affects the regulation of the reproductive neuroendocrine system through activation of the ER and AROM pathways. Moreover, since BPF and bisphenol S induced toxic and reproductive neuroendocrine effects similar to those of BPA, the current accepted usage of BPA and its analogs should be reconsidered in the future. Display omitted •Low levels of BPF led to increased expression of reproductive neuroendocrine-related genes.•BPF increased hormone levels of ACTH, GnRH, LH, FSH in brain and VTG in liver of zebrafish.•BPF affects reproductive neuroendocrine system through the ER and AROM pathways.•BPF and BPS induced similar toxic and reproductive neuroendocrine effects to those of BPA.