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Earlier recommendations advocated treatment of the cobalamin C defect with a combined approach that utilizes vitamin B12 plus betaine to provide a substrate for the conversion of homocysteine into methionine through betaine-homocysteine methyltransferase, and folic acid to enhance the remethylation pathway (164)

The prevalence of its reduced form in cells is due to the activity of glutathione reductase, which is both constitutive and inducible in response to oxidative stress