Abstract

We read with great interest the letter by Hubner et al. (1) on the stability of plasma sulfur-containing metabolites in the presence of anticoagulants (EDTA and citrate) and a homocysteine stabilizer. These authors observed time-dependent increases in plasma concentrations of homocysteine (Hcy)1 and similar increases in plasma S -adenosylhomocysteine (SAH) in EDTA- and citrate-containing whole blood after 24 h at room temperature. In discussing the mechanisms of these increases, they postulated that plasma Hcy is generated from SAH in erythrocytes by the SAH-hydrolase–catalyzed reaction, and Hcy and SAH leak into plasma from erythrocytes (1). They further noted that the inhibition of SAH hydrolase by citrate results in a smaller Hcy increase compared with EDTA, which they claimed does not inhibit this enzyme. We recently reported the iron-dependent in vitro chemical formation of Hcy from methionine (Met), SAH, and cystathionine, where EDTA or …

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