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Homocystine solubility and vascular disease
Author(s) -
Ragone Raffaele
Publication year - 2002
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.01-0682hyp
Subject(s) - homocysteine , chemistry , cystine , medicine , vascular disease , endocrinology , thrombosis , cysteamine , endothelial dysfunction , biochemistry , cysteine , enzyme
There is evidence that mild elevations of tHcy are associated with an increased risk for occlusive vascular disease, thrombosis, and stroke. It is hypothesized here that cellular toxicity could indirectly result from auto‐oxidation of homocysteine to homocystine. Elevated levels of total plasma homocysteine could be the primary cause of increased vascular risk, causing endothelial damage through a mechanism similar to that of cystine precipitation, which is known to cause stone formation in cystinosis and cystinuria. In fact, only traces of homocysteine circulate in plasma as the free thiol; the remainder is present as oxidation products. Of these, the symmetric disulfide homocystine is scarcely soluble at neutral pH. Its saturation limit is so close to the concentration of homocysteine in normal plasma that a transient increase of homocysteine levels could lead to precipitation of homocystine microcrystals in the bloodstream. These could damage endothelial tissue, acting as a mechanic primer for subsequent prothrombotic blood vessel alterations.—Ragone, R, Homocystine solubility and vascular disease. FASEB J. 16, 401–404 (2002)