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USING THE MEDAKA EMBRYO ASSAY TO INVESTIGATE DEVELOPMENTAL ETHANOL TOXICITY.
Citation:
OXENDINE, S., D. E. HINTON, J. COWDEN, AND S. J. PADILLA. USING THE MEDAKA EMBRYO ASSAY TO INVESTIGATE DEVELOPMENTAL ETHANOL TOXICITY. Presented at Society of Toxicology, San Diego, CA, March 05 - 09, 2006.
Description:
Ethanol (EtOH) is a well-known developmental toxicant that produces a range of abnormal phenotypes. While the toxic potential of developmental EtOH exposure is well characterized, the effect of the timing of exposure on the extent of toxicity remains unknown. Fish models such as the Japanese medaka, Oryzias latipes, provide a convenient system for investigating the effects of developmental EtOH exposure. In this study, medaka embryo toxicity tests were used to assess temporal variations in EtOH toxicity. Fertilized eggs were collected at the 64-cell stage and incubated during early, middle or late gestation (e.g., 0-3, 3-6 or 6-9 days post fertilization) with various sublethal concentrations of EtOH (0.1, 0.5 or 1%) (n=20 per dose). Viable embryos were photographed on the day of hatching and time to hatch, outer eye distance and total body length were used to assess toxicity. Dose-related hatching delays and growth inhibition were consistently observed in treated embryos (e.g., approximately 45% of controls hatched by day 9, whereas only 17% of embryos treated with 1% EtOH hatched by that time). Hatching delays were most pronounced when exposures occurred early in development. EtOH-induced growth inhibition, however, appeared to be most pronounced when exposures occurred late in development (e.g., 1% EtOH only decreased total body length by 8.8% if exposure occurred on days 0-3, but that decrement doubled to 17.6% when exposure occurred on days 6-9). The observed temporal variations in EtOH-induced growth inhibition may be related to stage-specific pharmacokinetic effects, as the EtOH dose was slightly higher in embryos treated late in development when compared to those treated earlier in development. In general, these data suggest that critical periods for heightened sensitivity to developmental EtOH exposure may vary according to the endpoint used to assess toxicity. This is an abstract of a proposed presentation and does not reflect EPA policy.