Pharmacodynamics of vitamin B12

1. Vitamin B12 is a red compound containing cobalt, which is required to be converted to methylcobalamin and coenzyme B12. Folic acid must be converted into dihydrofolate by reduction in the body, and then become tetrahydrofolate under the action of dihydrofolate reductase. Methylcobaltamine converts tetrahydrofolate to N5,N10-methenyltetrahydrofolate, which has the effect of supplying a "monocarbon group" during uracil deoxynucleotide conversion. N5,N10-methenyltetrahydrofolate reductase catalyzes the reduction of N5,N10-methenyltetrahydrofolate to N5-methylenic tetrahydrofolate. With the participation of methylcobaltamine, N5-methylalkenyltetrahydrofolate is decarboxylated to tetrahydrofolate, and the alkenyl is transferred to homocysteine ​​to form methionine. In this way, a sufficient amount of tetrahydrofolate must be maintained in the body for a large amount of DNA synthesis. Therefore, when vitamin B12 is deficient, its hematological effect is similar to that of folic acid, that is, DNA synthesis is blocked, resulting in megaloblastic anemia. Therefore, vitamin B12 is indirectly involved in the synthesis of thymidine.
2. The conversion of odd-numbered carbon fatty acids and methylmalonyl-CoA produced by oxidation of certain amino acids to succinyl-CoA must involve methylmalonyl-CoA mutase and coenzyme B12. When the body is deficient in vitamin B12, it can cause an increase in methylmalonic acid excretion and abnormal fatty acid metabolism. If methylmalonic acid is deposited in the nervous tissue, it may be denatured.
3. S-adenosylmethionine and methionine are mainly formed by homocysteine ​​receiving a methyl group of N5-methyltetrahydrofolate. Methyl vitamin B12 is a coenzyme of the above reaction. Therefore, the lack of vitamin B12 can lead to the synthesis of methionine and S-adenosylmethionine, which is probably one of the causes of neurological diseases.