Gonadal aryl hydrocarbon hydroxylase in rats and mice.

Rat and mouse gonadal aryl hydrocarbon hydroxylase (AHH) activity was measured and characterized in control and 3-methylcholanthrene (MC)-treated animals. The ovarian AHH activity increased 2to 3-fold in SpragueDawley, Lewis, and Brown-Norway rats following MC treatment. The same treatment decreased the testicular AHH activity in Sprague-Dawley rats. The induction of AHH activity after MC administration was the same in ovaries from weanling and adult Sprague-Dawley rats. Ovarian AHH activity was located in the microsomal frac tion, required NADPH, and had a broad pH optimum between 7.0 and 8.8. Both carbon monoxide and antibody to cytochrome c reducÃ-aseinhibited the ovarian AHH activity, suggesting that the hydroxylase is a cytochrome P-450-dependent monooxygenase. Basal testicular and ovarian AHH activity was similar in C57BL/6N (B6) and DBA/2N mice; however, after MC treatment an increase in gonadal AHH activity was ob served only in B6 mice. Treatment with 2,3,7,8-tetrachlorodibenzo-p-dioxin resulted in an increase in testicular AHH activity in both B6 and DBA/2N mice. The oocyte toxicity of MC in mice and rats was different. Seven days after a single i.p. injection of MC, 80 mg/kg, 87% of the primordial oocytes were destroyed in the ovaries of B6 mice, 69% were destroyed in DBA/2N mice, and none were destroyed in Sprague-Dawley rats. These data suggest that the oocyte toxicity of MC in the mouse is related to the ovarian AHH activity, whereas no associ ation is found between the ovarian AHH activity and oocyte toxicity in the rat.