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 gonadal development in fish and wildlife, and o,p′-DDT has been shown to be an relatively potent estrogen agonist. In this study, we exposed Japanese medaka (Oryzias latipes) to o,p′-DDT using two exposure protocols: direct exposure of early life stages to aqueous solutions from 1 to 100 d posthatch and exposure of female medaka to aqueous solutions, followed by mating with unexposed males to produce offspring that were exposed through mechanisms of maternal transfer. In treatments with direct aqueous exposures, an intersex condition of the gonad (testis-ova) was observed in male medaka exposed at early life stages to nominal o,p′-DDT concentrations of 50, 10, and 5 μg/L, indicating that this estrogen agonist can alter gonadal development when exposure occurs continuously over the period of gonadal differentiation. Comparisons with previously published data on the induction of testis–ova by exposure to nonylphenol (NP) and octylphenol (OP) indicated that the relative potencies for induction of intersex in medaka are o,p′-DDT > NP ≈ OP, which is not consistent with the relative estrogenic potencies of 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 offspring, although there was some delay in time to hatch of the offspring. Medaka exposed by maternal transfer showed no other toxicological responses during early life stages, but when treated fish reached sexual maturity, the females showed more advanced development of oocytes. In addition, when medaka exposed by maternal transfer were subsequently exposed at 10 months of age to 17β-estradiol (12 mg/L), there was a significantly greater induction of hepatic vitellogenin in DDT-exposed males in comparison to control males, indicating that exposure to estrogenic chemicals during early life stages may potentiate vitellogenin induction following exposure events later in the life of the fish.