Abstract
Summary
Liver microsomes of eight species (Holtzman- and Warfarin-resistant rats, mice, guinea pigs, hamsters, rabbits, calves, pigs, and chickens) have been assayed for the vitamin K-dependent carboxylase activity that converts protein-bound glutamyl residues to γ-carboxyglutamyl residues. Development of hypoprothrombinemia by anticoagulant treatment or vitamin K deficiency caused a two- to fourfold increase in liver carboxylase activity in all species except the guinea pig. The carboxylase activity in the hamster was about threefold higher than rat or guinea pig and, five- to sixfold higher than that of mice, rabbit, and pig. Microsomes from chicken or calf liver had very low vitamin K-dependent peptide carboxylase activity.
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