Methods for measuring sulfur amino acid metabolism.

Abstract

The importance of sulfur amino acid metabolism has become increasingly apparent in recent years. Methionine and cysteine are precursors of glutathione, which plays an important role in intracellular antioxidant/free radical defenses. Homocysteine is a non-protein-bound sulfur amino acid strongly implicated in the pathogenesis of several diseases. Both glutathione and homocysteine are affected by abnormalities in sulfur amino acid metabolism that occur in the clinical setting. The Storch-Young model, which determines methionine turnover and homocysteine remethylation by means of a tracer methionine infusion, has been improved by using plasma homocysteine (rather than methionine) enrichment in the model. A complex new tracer method involving the use of tracer serine, methionine, and leucine has been described to determine the effects of folate or pyridoxine deficiency on sulfur amino acid-methyl transfer reactions in humans. The etiology of hyperhomocysteinemia in chronic renal failure is controversial; new concepts in this area are described. There is new interest in the subspecies of homocysteine in the circulation. A new method is described for measuring the extremely low plasma concentrations of reduced homocysteine, using gas chromatography-mass spectrometry. Plasma S-adenosylhomocysteine, measured by fluorescence high-performance liquid chromatography, has been suggested as being superior to homocysteine as a predictor of the risk of vascular disease. This review highlights and critiques the above recent developments, and points out some of the complexities and pitfalls in designing and interpreting human metabolic studies involving the sulfur amino acids.