Vitamin K

A family of compounds found in plants, fish oils, and meats.

Good sources: Green leafy veggies, fruit (esp. strawberries), spinach, cabbage, egg yolks, fish, liver, and dairy products. A large portion of vitamin K is also produced by flora in the intestines. In fact, prolonged treatment with wide-spectrum antibiotics can decrease blood coagulation. Some 2nd generation cephalosporins (cefoperazone, cefamandole, and moxalactam) can also cause this effect (probably due to a warfarin like mechanism).

RDA: No RDA has been set but 70-40 mg per day appears to be adequate.

Functions: Formation of blood clotting agents (prothrombin, factor IX). It can be re-used.

• Formation of g-carboxyglutamate- The proteins for prothrombin and the clotting factors VII, IX, and X are formed as inactive precursors. Carboxylation of glutamate residues forms a mature clotting factor that contains γ-carboxyglutamate (Gla). This carboxylation is dependant upon vitamin K. Dicumarol, a naturally occuring anti-coagulant found in spoilt sweet clover, and warfarin, a synthetic analog of vitamin K, both inhibit the formation of Gla.
• Interaction of prothrombin with platelets- The Gla residues contain carboxyl groups (which are negatively charged). These carboxyl groups attract calcium ions (positively charged) which are then able to interact with the phospholipid membranes of platelets.
• Rold of γ-carboxyglutamate residues in other proteins- These Gla residues are also present in other proteins but the role of vitamin K in their synthesis is not clear.

Deficiency: Hemorrhage. Infants are given an injection of vitamin K at birth. Their intestines are sterile and they cannot have vitamin K produced (hence the injection). However, deficiency is rare in the adult because of the large amount synthesized by intestinal bacteria.

Toxicity: Toxic to the membrane of RBC’s at high doses. Long-term, high-dose administration can cause jaundice and hemolytic anemia.