AbstractEmbryos of the Japanese medaka were individually exposed to varying concentrations of 3H2,3,7,8‐tetrachlorodibenzo‐p‐dioxin (TCDD) in a static, nonrenewal system. The EC50 with 95 confidence interval (C.I.) to prevent hatching was 14 (11–17) nanograms (ng) of TCDD equivalents per liter (L) of water (parts per trillion). The LC50 with 95 C.I. for survival to 3 d posthatch was 9 (6–12) ng TCDD equivalents/L. The EC50 with 95 C.I. for embryos with minor lesions and severe, life‐threatening lesions were 3.5 (1.3–5.7) ng TCDD equivalents/L and 14 (12.4–15.6) ng TCDD equivalents/L, respectively. In a separate experiment that was terminated prior to the embryos hatching or dying, the EC50 for lesions was calculated to be 2.2 (1.4–3.0) ng TCDD equivalents/L. Based on the amount of TCDD equivalents recovered from dechorionated embryos, the ED50 with 95 C.I. for lesions was calculated to be 0.24 picograms of TCDD equivalents per milligram of dechorionated embryo weight (parts per billion). When the embryos were exposed to 3HTCDD within 1 to 2 h after fertilization, no concentration dependent increase in visible lesions was observed until after the formation of the liver rudiment (day 4 of development). By exposing Japanese medaka embryos to lethal concentrations of TCDD beginning on different days of embryonic development, it was demonstrated that the sensitive period for toxicity was during liver formation on day 4 or 5 of development. The sensitive period for development was not caused by differences in TCDD absorption across the chorion. When embryos were exposed to 3HTCDD prior to, during or after liver formation, there was no statistical difference in the dose of TCDD equivalents that crossed the chorion and entered th
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