Transient exposure of brown trout embryos from fertilization until hatch (70 days) to 17β-estradiol (E2) was investigated. Embryos were exposed to 3.8 and 38.0. ng/L E2 for 2. h, respectively, under four scenarios: (A) exposure once at the day of fertilization (0 days post-fertilization, dpf), (B) once at eyeing stage (38. dpf), (C) weekly exposure until hatch or (D) bi-weekly exposure until hatch. Endpoints to assess estrogen impact on embryo development were fertilization success, chronological sequence of developmental events, hatching process, larval malformations, heart rate, body length and mortality.Concentration-dependent acceleration of development until median hatch was observed in all exposure scenarios with the strongest effect observed for embryos exposed once at 0. dpf. In addition, the hatching period was significantly prolonged by 4-5 days in groups receiving single estrogen exposures (scenarios A and B). Heart rate on hatching day was significantly depressed with increasing E2 concentrations, with the strongest effect observed for embryos exposed at eyeing stage. Estrogenic exposure at 0. dpf significantly reduced body length at hatch, not depending on whether this was a single exposure or the first of a series (scenarios A and D).The key finding is that even a single, transient E2 exposure during embryogenesis had significant effects on brown trout development. Median hatch, hatching period, heart rate and body length at hatch were found to be highly sensitive biomarkers responsive to estrogenic exposure during embryogenesis. Treatment effects were observable only at the post-hatch stage.