RESUMO
Early life-stage exposure of fishes to endocrine disrupting chemicals can induce reproductive impairment at sexual maturity. Previously, we demonstrated decreased fecundity of Japanese medaka (Oryzias latipes) exposed via maternal transfer to the novel brominated flame retardant, 1,2,5,6-tetrabromocyclooctane (TBCO). However, that study failed to identify the causative mechanism. In other studies we have shown that decreased fecundity of adult fish exposed to dietary TBCO is likely due to impaired oocyte maturation. The goal of the present study was to determine if impaired oocyte maturation is responsible for decreased fecundity of Japanese medaka exposed as embryos to TBCO, via maternal transfer. Sexually mature fish (F0) were fed either a control diet or a low (74.7 µg/g) or high (663 µg/g) diet containing TBCO for 21 days. Eggs (F1) were collected during the final week of exposure and reared to sexual maturity at which point fecundity was assessed using a 21-day reproduction assay. Upon termination of the assay, an ex vivo oocyte maturation assay was used to determine whether maturation inducing hormone (MIH) stimulated oocyte maturation was impaired. Additionally, concentrations of 17ß -estradiol (E2) in blood plasma and expression of genes involved in vitellogenesis and oocyte maturation were quantified. The F1 generation females reared from the low or high F0 treatments experienced a 26.0 % and 56.8 % decrease in cumulative fecundity, respectively. Ex vivo MIH stimulated oocyte maturation from the low and high TBCO treatments were decreased by 23.4 % and 20.0 % respectively. There was no significant effect on concentrations of E2. Transcript abundance of vtgI was significantly decreased in a concentration dependent manner. Transcript abundance of mPRα, pgrmc1, pgrmc2, and igf3 were decreased but effects were not statistically significant. Overall, results suggest that impaired oocyte maturation causes decreased fecundity of Japanese medaka exposed to maternally deposited TBCO.