Vitamin K: Function and Effects of Deficiency

Vitamin K is known as the antihemorrhagic vitamin because it promotes blood coagulation. In 1929, Dam observed that newly hatched chicks develop a fatal hemorrhagic disease when raised on a ration adequate in all known vitamins and dietary essentials.

The factor missing from diet was present in the unsaponifiable nonsterol fraction of hog liver and of alfalfa. In 1935, the same investigator showed that the antihemorrhagic factor was associated with decrease in the prothrombin concentration in the blood.

Subsequent research led to the isolation and identification of vitamin K in 1939. There are at least two naturally occurring substances, vitamin K1 and K2, capable of preventing hemorrhagic diathesis due to lowered prothrombin levels. Vitamin K1 was isolated from alfalfa and K2 was isolated from fish meal.

Many related compounds also have vitamin K activity. A synthetic compound, 2-methyl-1,4-naphthoquinone, is more potent than natural vitamin K. Menadione, the principle form of the vitamin used for clinical purposes, is used as the reference standard for measurement of vitamin K activity.

Vitamin K is fat soluble and relatively stable to heat, oxygen and moisture, but is destroyed by sunlight and alkalies. There is little or no destruction of the vitamin during food processing.

The exact biochemical function of vitamin K is not known. However, a well established symptom of vitamin K deficiency is defective blood coagulation: more specifically, vitamin K is required to maintain normal plasma levels of prothrombin and three other clotting factors (V11, 1X, and X). A reduction of any of these four factors, presumably all proteins, may be used to measure the action of vitamin K.

The finding also indicates that vitamin K also participates in oxidative phosphorylation and in mitochondrial electron transport.

Absorption of vitamin is dependent upon the presence of bile salts in the upper intestinal tract. After absorption, it is transported to the liver where it catalyzes the synthesis of prothrombin (factor 11).

Consequently, any disease or injury that obstructs the flow of bile, or damages the liver in such a manner that synthesis of prothrombin is inhibited, will cause a reduction in prothrombin. Since the blood-clotting process depends on the conversion of fibrinogen to fibrin by the action of thrombin, the active form of prothrombin, decrease prothrombin formation will increase clotting time.
Vitamin K: Function and Effects of Deficiency