• 5C-aglycone metabolite;
  • CEHC;
  • menaquinone;
  • phylloquinone;
  • tocopherol

The mechanisms by which vitamin E interferes with vitamin K activity, especially blood clotting, are not known, but hypothetically this interference may involve metabolic pathways. Phylloquinone (K1) must be converted to menaquinone (MK-4, the most potent extrahepatic tissue vitamin K) by truncation of the K1 side chain and replacement with geranylgeranyl. Possible mechanisms for the vitamin E and K interaction include: 1) vitamin E competes for the yet undiscovered enzyme that truncates the K1 side chain; 2) vitamin E competes with K1 for the hypothetical cytochrome P450 enzyme that ω-hydroxylates the K1 side chain, thereby preventing its β-oxidation and its removal for MK-4 formation; or 3) vitamin E increases xenobiotic pathways that increase hepatic metabolism and excretion of all vitamin K forms. Currently, the pathway for K1 conversion to MK-4 is unknown, the process for regulating vitamin K metabolism to urinary excretion products is unknown, and why vitamin E supplements have such a dramatic effect, causing bleeding in some individuals and not in others, remains a mystery.