Vitamin K Deficiency and Oxidative Phosphorylation

Abstract

Severe vitamin K deficiency in the rat, produced by strictly nutritional means, does not impair the efficiency of oxidative phosphorylation in liver mitochondria, with either glutamate or β-hydroxybutyrate as substrate. Liver mitochondria from dicumarol-treated rats also exhibited a normal coupling of phosphorylation to oxidation. In vitro addition of vitamin K₁ or K₂ to liver mitochondria from vitamin K-deficient or dicumarol-treated rats with occasional low P/O ratios, did not restore the P/O ratio to maximal values. In vitro uncoupling of oxidative phosphorylation by dicumarol was not reversed by vitamin K₁. It does not appear that vitamin K exerts its action on prothrombin synthesis through participation in mitochondrial oxidative phosphorylation.