*Background* 
Based on previous findings, we have estimated that, in injured coronary artery tissue, the low molecular weight disulfides homocystine and cysteine-homocysteine, otherwise identified as oxidized homocysteine equivalents (OHcyE), may achieve a total concentration that is higher than the aqueous solubility of homocystine at room temperature. In order to verify whether or not OHcyE could reach their saturation limit in the vascular tissue, we have measured the solubility of homocystine in physiological-like condition.

*Materials and methods* 
The solubility of homocystine has been measured in aqueous sodium chloride solutions at 37 °C by differential pulse polarography based on the reduction of homocystine to homocysteine.

*Results* 
We have estimated that the concentration achieved by OHcyE in injured coronary artery tissue is at least near-saturating, because the solubility of homocystine in physiological-like condition, above which deposition of homocystine and/or cysteine-homocysteine as solid phase occurs, almost exactly matches its value. Near-saturation levels of OHcyE within the vascular tissue means that significant leakage of intracellular fluid can promote OHcyE crystallization in tissue fluids, which may serve to initiate inflammation. 

*Conclusions* 
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
