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Homocystine solubility and vascular disease

Department of Biochemistry and Biophysics-CRISCEB, Second University of Naples, 80138 Naples, Italy

¹Correspondence: Department of Biochemistry and Biophysics-CRISCEB, Second University of Naples, via Costantinopoli 16, 80138 Naples, Italy. E-mail: ragone@unina2.it or raffrag{at}tiscali.it

ABSTRACT

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.

Key Words: homocysteine • cystine solubility • redox thiol status

This article has been cited by other articles:

				A. B. Sobol, E. Bald, and J. Loba Fractions of Total Plasma Homocysteine in Patients with Ischemic Stroke Before the Age of 55 Years Angiology, March 1, 2005; 56(2): 201 - 209. [Abstract] [PDF]