Pharmacology of vitamin b12
 Pharmacodynamics
 ① vitamin B12 containing cobalt as a red compound, to be converted to methyl cobalamin and coenzyme B12 after a activity. Folic acid in the body must be restored into the role of dihydrofolate, then under the action of dihydrofolate reductase, a folate. Methyl cobalamin can tetrahydrofolate into N5, N10-methylene tetrahydrofolate base, which is transformed in the process of uracil nucleotide has a supply of "a carbon-based group" role. N5, N10-methylene tetrahydrofolate reductase catalyzes the base N5, N10-methylene tetrahydrofolate base, so a reduction of N5-alkenyl tetrahydrofolate. Participation in the methyl cobalamin, N5-A alkenyl methylene tetrahydrofolate off base, then into tetrahydrofolate, and methylene base is transferred to homocysteine to form methionine. This body must maintain an adequate amount of folate, for a large number of DNA synthesis. Therefore, the lack of vitamin B12, its impact on hematology and folic acid similar to that blocked DNA synthesis, resulting in megaloblastic anemia. Therefore, vitamin B12 indirectly involved in the thymidine nucleotide synthesis.

 ② odd carbon fatty acids and certain amino acid oxidation of methyl malonyl coenzyme A into succinyl coenzyme A must have methyl malonyl coenzyme A mutase and coenzyme B12 participation. When the body lacks vitamin B12, can cause increased excretion of methylmalonic acid and fatty acid metabolism. If calm methylmalonic acid in nerve tissue, which may cause the degeneration.

 ③ S-adenosylmethionine and methionine mainly by homocysteineto accept N5-methyl-methyl tetrahydrofolate formed. Methyl vitamin B12 is the reaction of the coenzyme. Therefore, the lack of vitamin B12 can lead to methionine and S-adenosylmethionine synthesis obstacles, nervous system disease is likely to be one of the reasons.