Following the ban of polybrominated diphenyl ether (PBDEs) flame retardants under well-documented toxicity issues, organophosphate such as tris(2-butoxyethyl) phosphate (TBOEP) and tris(2-cloroethyl) phosphate (TCEP) were considered as potential substitutes. Although TBOEP and TCEP are consistently detected in the aquatic environment, there are few data about the possible toxicological effects of these compounds on aquatic organisms, including fish. In the present study, we have investigated the influence of TBOEP and TCEP on neuro- and interrenal steroidogenesis of juvenile Atlantic salmon (Salmo salar), after a seven-day exposure to four different concentrations (0 (control), 0.04, 0.2 and 1 mg/L) of each compound. TBOEP and TCEP were diluted in Milli-Q water. The expression of genes involved in steroidogenesis (StAR, cyp19a, cyp19b, cholesterol side-chain cleavage enzyme (P450scc), 3β-hydroxysteroid dehydrogenase (3β-hsd), and 11β-hydroxylase (cyp11β)), were analyzed in the brain and head kidney using real-time PCR. Plasma 11-ketotestosterone (11-KT) analysis was performed using enzyme immunoassay (EIA). Our results showed that TBOEP accumulated more rapidly than TCEP in fish muscle tissue. Surprisingly, TBOEP produced less pronounced effects than TCEP on neural and interrenal steroidogenic responses, despite the observed rapid uptake and bioaccumulation pattern. Specifically, TBOEP produced significant and consistent concentration-specific alterations on neural- and interrenal steroidogenesis. Plasma levels of 11-KT were not significantly altered by any of the exposures. The increased expression of steroidogenic genes demonstrated in the present study could produce time-specific alterations in the production of glucocorticoids and steroid hormones that play integral roles in fish metabolism, stress responses and adaptation, sexual maturation, reproduction and migration with overt consequences on reproductive success and survival.