Methylcobalamin (Vitamin B12)

Methylcobalamin, or vitamin B12, is found in fish, shellfish, meats, and dairy products. Although the two terms used interchangeably, vitamin B12 is also available as hydroxocobalamin, a less commonly prescribed drug product. Methylcobalamin is used to treat pernicious anemia and vitamin B12 deficiency, as well as to determine vitamin B12 absorption using the Schilling test. B12 deficiency in healthy individuals is rare; the elderly, those with vegan diets, and patients with malabsorption problems are more likely to experience this problem. If vitamin B12 deficiency is not treated with supplementation, then anemia, intestinal problems, and nerve damage may occur.

Methylcobalamin is a water-soluble, organometallic compound with a trivalent cobalt ion bound inside a corrin ring. The central metal ion is Co (cobalt). Plants and animals do not have the enzymes to synthesize methylcobalamin; only bacteria and archaea can do this. Higher plants do not concentrate methylcobalamin from the soil, human dietary B12 needs are better met with animal then plant tissues.

Mechanism of Action

Vitamin B12 is used in the body in two forms, methylcobalamin and 5-deoxyadenosyl cobalamin. The enzyme methionine synthase needs methylcobalamin as a cofactor. This enzyme is involved in the conversion of the amino acid homocysteine into methionine which is, in turn, required for DNA methylation.

5-deoxyadenosylcobalamin is a cofactor needed by the enzyme that converts L-methylmalonyl-CoA to succinyl-CoA, an extraction that allows an organism to gain energy from proteins and fats. Furthermore, succinyl CoA is required for the production of hemoglobin, the substance that allows oxygen to be carried by red blood cells.


Methylcobalamin is essential to growth, cell reproduction, hematopoiesis, and nucleoprotein and myelin synthesis. Cells characterized by rapid division appear to require methylcobalamin the most. Vitamin B12 can be converted to coenzyme B12 in tissues; in the absence of coenzyme B12, tetrahydrofolate cannot be regenerated from its inactive storage form, 5-methyl tetrahydrofolate, resulting in functional folate deficiency. Vitamin B12 also may be involved in maintaining sulfhydryl (SH) groups in the reduced form required by many SH-activated enzyme systems. Through these reactions, vitamin B12 is associated with fat and carbohydrate metabolism and protein synthesis. Vitamin B12 deficiency results in megaloblastic anemia, GI lesions, and neurologic damage (which begins with an inability to produce myelin and is followed by gradual degeneration of the axon and nerve head). Vitamin B12 requires an intrinsic factor-mediated active transport for absorption; A lack of or inhibition of intrinsic factor leads to pernicious anemia.

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