Figure 1.

The metabolization of homocysteine (Hct) in the body. Hct is formed by transmethylation of methionine via S-adenosylmethionine (SAM) and S-adenosylhomocysteine (SAH) by methionine adenosyltransferase (MAT) (transmethylation pathway). Hct can be remethylated to methionine (remethylation pathway) or transsulfurated to cystathionine and cysteine (transsulfuration pathway). The transsulfuration pathway requires the catalysis of vitamin B₆-dependent cystathionine beta-synthase (CβS). The remethylation of Hct to methionine is catalyzed by the vitamin B₁₂-dependent methionine synthase (MS). Tetrahydrofolate (THF) is recycled to form 5-methyltetrahydrofolate (5-MTHF), catalyzed by 5,10-methylenetetrahydrofolate reductase (MTHFR). Folic acid can be used as a primary substance to produce 5-MTHF, and 5-MTHF could produce methionine and Hct. Thus, the reduction of folic acid could lead to hyperhomocysteinemia (HHct).