Vitamin K in Biochemistry

Prothrombin and clotting factors II, VII, IX, X require carboxylation of their glutamic acid (Glu) residues.

Carboxylation results in the formation of γ-carboxyglutamate (Gla) in mature prothrombin and clotting factors.

Vitamin K is essential for the carboxylase enzyme involved in the carboxylation reaction.

Dihydroquinone form of vitamin K is necessary for the carboxylation process.

Vitamin K functions in the coagulation process by binding calcium and phospholipids on the surface of platelets.

Warfarin is a competitive inhibitor of vitamin K reductase, prolonging coagulation time.

Osteocalcin, a bone turnover protein, requires γ-carboxyglutamate for binding to hydroxyapatite in the bone.

Vitamin K deficiency is rare due to intestinal bacterial synthesis, but can be caused by lipid malabsorption, antibiotic therapy, and gastrointestinal infections.

Vitamin K deficiency can lead to high blood calcium levels, heart problems, and hemorrhagic symptoms.

Large doses of vitamin K can cause hemolytic anemia and jaundice due to toxic effects on red blood cell membranes.

Vitamin K is synthesized by the liver and requires an additional carboxyl group for calcium binding.

Oral antibiotic therapy can cause functional vitamin K deficiency by inhibiting bacterial synthesis.

Vitamin K is a cofactor for the conversion of prothrombin to thrombin.

Vitamin K is required for γ-carboxylation of glutamic acid residues.

Sources of Vitamin K include green leafy vegetables, certain vegetable oils, and synthesis by intestinal bacteria.

Vitamin K is essential for proper blood clotting and bone metabolism.

Prothrombin and clotting factors II, VII, IX, X require carboxylation of their glutamic acid (Glu) residues.

Carboxylation results in the formation of γ-carboxyglutamate (Gla) in mature prothrombin and clotting factors.

Vitamin K is essential for the carboxylase enzyme involved in the carboxylation reaction.

Dihydroquinone form of vitamin K is necessary for the carboxylation process.

Vitamin K functions in the coagulation process by binding calcium and phospholipids on the surface of platelets.

Warfarin is a competitive inhibitor of vitamin K reductase, prolonging coagulation time.

Osteocalcin, a bone turnover protein, requires γ-carboxyglutamate for binding to hydroxyapatite in the bone.

Vitamin K deficiency is rare due to intestinal bacterial synthesis, but can be caused by lipid malabsorption, antibiotic therapy, and gastrointestinal infections.

Vitamin K deficiency can lead to high blood calcium levels, heart problems, and hemorrhagic symptoms.

Large doses of vitamin K can cause hemolytic anemia and jaundice due to toxic effects on red blood cell membranes.

Vitamin K is synthesized by the liver and requires an additional carboxyl group for calcium binding.

Oral antibiotic therapy can cause functional vitamin K deficiency by inhibiting bacterial synthesis.

Vitamin K is a cofactor for the conversion of prothrombin to thrombin.

Vitamin K is required for γ-carboxylation of glutamic acid residues.

Sources of Vitamin K include green leafy vegetables, certain vegetable oils, and synthesis by intestinal bacteria.

Vitamin K is essential for proper blood clotting and bone metabolism.