Intracellular Distribution of Estrogen Inactivating Mechanism in Rat Liver and Other Tissues.

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Abstract
Rat liver homogenate was separated into nuclei, mitochondria, microsomes and supernatant by differential centrifugation. Homogenate, fractions and combinations of fractions were studied for ability to decrease the activity of estradiol, estrone or diethylstilbestrol (DES) when incubated at 38[degree]C for 2 hrs. in the presence of DPN and nicotinamide. Uteri of ovariectomized mice were used to determine the amt. of biological activity remaining. No single fraction decreased the estradiol activity markedly. Microsomes and supernatant, when recombined, were comparable to homo-genates in ability to inactivate estradiol. Though kidney or salivary gland homogenate was inert, the supernatant of either when combined with liver microsomes effectively inactivated estradiol. Supernatant could also be replaced by riboflavin monophosphate (RMP). The microsomes of kidney or of salivary glands when used with liver supernatant failed to inactivate estradiol. The inactivation of estrone occurred with the same liver fractions necessary for estradiol: microsomes and supernatant. No appreciable inactivation occurred with any single fraction. For the in vitro inactivation of DES, liver supernatant alone was almost as effective as homogenate. Kidney supernatant was ineffective. RMP alone, in the absence of any tissue, destroyed the estrogenic activity of DES. A non-enzymatic inactivation of DES by liver tissue was also indicated.