Abstract
AbstractOal dosesof 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin (TCDD) were administered twice within 7 d (total concentration 0.01, 0.1, 1, 10, or 100 μg TCDD/kg body weight) to flounder (Platichthys flesus). After 10 d of exposure, flounder were sacrificed, and the effects of TCDD exposure on hepatic microsomal total cytochrome P450 content, 7‐ethoxyresorufin‐O‐deethylase (EROD) activity, and glutathione‐S‐transferase activity were examined. In addition, plasma and hepatic retinoid and plasma thyroid hormone levels were analyzed. Overall a good correlation existed between the dose and liver concentrations of TCDD. However, only 0.75% of the total dose of TCDD was retained in the flounder liver. The TCDD caused a dose‐related, statistically significant induction of the hepatic microsomal total cytochrome P450 content (4.4‐fold; p < 0.001) and associated EROD activity (27‐fold; p < 0.001), without obvious changes in body weight, liver weight, and condition factor. Total glutathione‐S‐transferase activity was not induced in livers of flounder exposed to TCDD. No TCDD‐induced changes in liver retinoid, plasma retinol, and plasma thyroid hormone parameters were observed. These results indicate that the flounder is an aryl hydrocarbon (Ah) receptor‐responsive species with respect to CYP1A induction but not with respect to other mammalian Ah receptor‐associated responses.
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