Affiliations: Dipartimento di Chimica, Università Federico II,
Naples, Italy | Dipartimento delle Scienze Biologiche, Università
Federico II, Naples, Italy
Note: [] Corresponding author: Raffaele Ragone, Dipartimento delle
Scienze Biologiche, Università Federico II, via Mezzocannone 16, 80134
Naples, Italy. Tel.: +39 081 253 6682; Fax: +39 199 707 0716582; E-mail:
raffrag@gmail.com
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.
