Excessive selenium (Se), especially selenite form exerts great toxicity to fish. Most studies have attached considerable attention to the adverse effects of Se on parental fish. However, the transgenerational toxicity of Se on fish has been rarely reported. In the present study, zebrafish embryos were exposed to environmentally relevant concentrations of Na₂SeO₃ (0, 12.5, 25, 50, and 100 μg/L) for 120 days. And the exposed zebrafish (F0) were allowed to spawn with normal zebrafish after sexual maturity. Subsequently, the offspring (F1) were cultured in clean water for 5 days. In the F0 generation, exposure to 100 μg/L Na₂SeO₃ significantly increased the Se content in the tissues (liver, brain and gonad) and decreased the body length and weight. After parental exposure to 100 μg/L Na₂SeO₃, the increased mortality, elevated malformation rate and reduced body length were measured in F1 zebrafish. The Se content was only significantly increased in F1 larvae derived from exposed females in the 100 μg/L exposure group. The contents of thyroid hormones (THs), growth hormone (GH) and insulin-like growth factor (IGF) significantly decreased in F0 and F1 zebrafish. The transcriptional levels of genes along the hypothalamic-pituitary-thyroid (HPT) axis and growth hormone/insulin-like growth factor (GH/IGF) axis were detected to further explore the possible mechanisms of Se-induced thyroid and growth hormone disruption. The results suggest that the toxicity of Se in zebrafish can be markedly transmitted to offspring. And the transgenerational development toxicity might be different due to the differences in gender of exposed parents.