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Oxidative phosphorylation in mitochondria from animals treated with 2-chloro-3-phytyl-1,4-naphthoquinone, an antagonist of vitamin K1

Biochemical and Biophysical Research Communications
Publication Date
DOI: 10.1016/0006-291x(62)90245-0
  • Biology


Abstract Possible function of certain quinones as coenzymes in the multienzyme system of the respiratory chain in electron transport and in oxidative phosphorylation has been considered repeatedly. Such a role for vitamin K was suggested first by Martius and Nitz-Litzow (1954a, 1954b), who reported a reduced efficiency of phosphorylation associated with the oxidation of β-hydroxybutyrate in mitochondria from vitamin K-deficient chicks. This defect could be corrected by the addition of vitamin K 1. Also, they observed that dicoumarol and other substances related to vitamin K could uncouple the phosphorylation associated with the oxidation of β-hydroxybutyrate ( Martius and Nitz-Litzow, 1953). It has been shown recently ( Lowenthal et al. 1960) that 2-chloro-3-phytyl-1,4-naphthoquinone, a structural analogue of vitamin K 1, is an antagonist of the effects of vitamin K 1 (2-methyl-3-phytyl-1,4-naphthoquinone) on blood coagulation. In the normal animal the antagonist causes an anticoagulant effect, reversible by vitamin K 1, and in the coumarin anticoagulant treated animal it inhibits the antidotal effect of vitamin K 1. Because of the above considerations it was of interest to investigate oxidative phosphorylation of liver mitochondria isolated from animals pretreated with the vitamin K 1 antagonist ( Parmar and Lowenthal 1961).

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