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Disease Markers
Volume 27, Issue 2, Pages 55-61
http://dx.doi.org/10.3233/DMA-2009-0649

Homocysteine Disulphides and Vascular Disease

Mauro Iuliano,1 Gaetano De Tommaso,1 and Raffaele Ragone2

1Dipartimento di Chimica, Università Federico II, Naples, Italy
2Dipartimento delle Scienze Biologiche, Università Federico II, Naples, Italy

Received 28 October 2009; Accepted 28 October 2009

Copyright © 2009 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

The total plasma concentration of homocysteine is a marker of this amino acid's atherogenic potential. However, the homocysteine pool exists almost entirely as oxidized homocysteine equivalents (OHcyE), composed of homocystine and cysteine-homocysteine disulphides (20–30%), and protein-bound disulphide (70–80%). We have noticed that the total concentration of OHcyE in injured coronary artery tissue is higher than the aqueous solubility of homocystine (∼1.4–1.5 × 10-3 mol kg-1 versus ∼0.6 mol kg-1). Based on the measurement of the solubility of homocystine in a plasma-mimetic condition (0.17 mol kg-1 NaCl at 37°C), we have estimated that OHcyE may really reach their saturation limit in the vascular tissue (0.93–1.02 × 10-3 mol kg-1), above which their deposition as solid phase may occur. This means that significant leakage of intracellular fluid can promote OHcyE crystallization in tissue fluids, which may serve to initiate inflammation. We speculate that deposition of OHcyE crystals could damage blood vessels and act as a primer of homocysteine-triggered inflammation, thus being along the causal pathway that leads to vascular dysfunction.