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.

中文翻译：

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同型半胱氨酸二硫化物和血管疾病。

同型半胱氨酸的总血浆浓度是该氨基酸致动脉粥样硬化潜力的标志。然而，同型半胱氨酸池几乎完全以氧化同型半胱氨酸等价物 (OHcyE) 形式存在，由同型半胱氨酸和半胱氨酸-同型半胱氨酸二硫化物 (20-30%) 和蛋白质结合的二硫化物 (70-80%) 组成。我们已经注意到，受损冠状动脉组织中 OHcyE 的总浓度高于同型半胱氨酸的水溶性（~1.4–1.5 × 10 ^-3 mol kg ^-1对~ 0.6 mol kg ^-1）。基于在血浆模拟条件（0.17 mol kg ^-1 NaCl 在 37°C 下）中高半胱氨酸溶解度的测量，我们估计 OHcyE 可能真的达到其在血管组织中的饱和极限（0.93-1.02 × 10^-3 mol kg ^-1 )，高于此值可能会发生固相沉积。这意味着细胞内液的大量泄漏可以促进组织液中的 OHcyE 结晶，这可能有助于引发炎症。我们推测 OHcyE 晶体的沉积可能会损伤血管并作为同型半胱氨酸引发炎症的引物，从而沿着导致血管功能障碍的因果途径。