Gonadal development and endocrine responses in Japanese medaka (Oryzias latipes) exposed to o,p '-DDT in water or through maternal transfer

Various isomers and metabolites of DDT disrupt endocrine systems and gonada l development in fish and wildlife, and o,p'-DDT has been shown to be an re latively potent estrogen agonist. In this study, we exposed Japanese medaka (Oryzias latipes) to o,p'-DDT using two exposure protocols: direct exposur e of early life stages to aqueous solutions from 1 to 100 d posthatch and e xposure of female medaka to aqueous solutions, followed by mating with unex posed males to produce offspring that were exposed through mechanisms of ma ternal transfer. In treatments with direct aqueous exposures, an intersex c ondition of the gonad (testis-ova) was observed in male medaka exposed at e arly life stages to nominal o,p'-DDT concentrations of 50, 10, and 5 mu g/L , indicating that this estrogen agonist can alter gonadal development when exposure occurs continuously over the period of gonadal differentiation. Co mparisons with previously published data on the induction of testis-ova by exposure to nonylphenol (NP) and octylphenol (OP) indicated that the relati ve potencies for induction of intersex in medaka are o,p'-DDT > NP approxim ate to OP, which is not consistent with the relative estrogenic potencies o f OP > NP > o,p'-DDT observed in the yeast estrogen screening (YES) assay. In the maternal transfer protocol, no testis-ova were observed in the offsp ring, although there was some delay in time to hatch of the offspring. Meda ka exposed by maternal transfer showed no other toxicological responses dur ing early life stages, but when treated fish reached sexual maturity, the f emales showed more advanced development of oocytes. In addition, when medak a exposed by maternal transfer were subsequently exposed at 10 months of ag e to 17 beta-estradiol (12 mg/L), there was a significantly greater inducti on of hepatic vitellogenin in DDT-exposed males in comparison to control ma les, indicating that exposure to estrogenic chemicals during early life sta ges may potentiate vitellogenin induction following exposure events later i n the life of the fish.