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      The effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on weight gain and hepatic ethoxyresorufin-o-deethylase (EROD) induction vary with ovarian hormonal status in the immature gonadotropin-primed rat model.

      Reproductive Toxicology (Elmsford, N.y.)
      Animals, Chorionic Gonadotropin, pharmacology, Cytochrome P-450 CYP1A1, biosynthesis, Diestrus, drug effects, Dose-Response Relationship, Drug, Drug Synergism, Environmental Pollutants, toxicity, Estradiol, analogs & derivatives, blood, Female, Gonadotropins, Equine, Humans, Liver, enzymology, Models, Animal, Ovariectomy, Ovary, pathology, Ovulation, Proestrus, Progesterone, Rats, Rats, Sprague-Dawley, Tetrachlorodibenzodioxin, Weight Gain

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          Abstract

          Immature female rats received 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) during an induced proestrus or diestrus. The inhibitory effect of TCDD on acute weight gain and the induction of hepatic ethoxyresorufin-o-deethylase (EROD) activity by TCDD were greatest during proestrus. In a second experiment, ovariectomized rats received estradiol cypionate (ECP) or progesterone followed by TCDD. TCDD and estradiol each alone significantly inhibited weight gain. Progesterone potentiated the effects of TCDD on weight gain. The highest dose of ECP was associated with greater induction of hepatic EROD activity by TCDD than seen with TCDD alone. Estradiol modulates the induction of hepatic EROD activity by TCDD. Differential effects of TCDD on acute weight gain during proestrus vs. diestrus in this model do not mimic changes induced by estrogen alone. Hepatic responses to TCDD may vary according to phase of the female reproductive cycle.

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