Homocysteine, a sulfur amino acid, is an important methionine derivative, w
hich has been implicated in the pathogenesis of atherothrombosis, Although
only observational, epidemiological studies are available at present, the e
vidence of an association between hyperhomocysteinemia and increased cardio
vascular risk is quite strong and this is confirmed also in a population of
chronic renal failure patients.
From a biochemical standpoint at least three mechanisms have been so far su
mmoned in order to explain homocysteine toxicity including: oxidation, hypo
methylation, and acylation. Proteins are believed to play a crucial role as
homocysteine molecular targets. Interference with the functions of several
of such macromolecules has been so far described being mediated by any of
the above mechanisms,
Vitamins may positively influence homocysteine metabolism, thus facilitatin
g the metabolic clearance of this compound. Therefore they are presently co
nsidered as potential means for reducing plasma levels of this amino acid a
nd preventing vascular occlusions in hyperhomocysteinemic patients. These c
ompounds, with special regard to folate, are eligible for interventional cl
inical trials, from which the definitive answer on the role of homocysteine
in atherothrombosis is expected. Copyright (C) 2000 S. Karger AG, Basel.