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Department of Biochemistry, University of Nebraska College of Medicine, Omaha, Nebraska 68105
The effect of sex hormones on vitamin K deficiency was studied in intact and castrated male and female rats. The onset of vitamin K deficiency after castration was enhanced in the female and retarded in the male. Castrated male and female rats developed vitamin K deficiency to about the same extent. Plasma prothrombin levels in castrated male and female rats fed vitamin K-deficient diet dropped after the injection of testosterone and rose or remained high after the injection of estradiol. Castration did not prevent hyperprothrombinemia in adult female rats fed adequate amounts of vitamin K. Phenobarbital, methyl cholanthrene and DDT, like testosterone, appeared to enhance the onset of vitamin K deficiency in castrated male rats; estradiol virtually prevented the onset of deficiency; and progesterone was without effect compared to uninjected controls. The activity of phylloquinone epoxidase in liver microsomes varied with the degree of vitamin K deficiency. Activity of the enzyme was highest when prothrombin levels in plasma were lowest. A proposal is made that prothrombin is formed more rapidly and at a lower effective concentration of vitamin K in female or estrogen-treated rats.
KEY WORDS: sex hormones vitamin K epoxidation prothrombin microsomes
1 Supported in part by Grant AM 14937 and Contract NICHD 72-2787 from the National Institutes of Health.
Manuscript received 16 August 1973.