Abstract
Over the last years, homocysteine has been recognized as an independent risk factor for atherosclerotic vascular disease (1). The known reasons for an increased level of plasma homocysteine are genetic defects of cystathionine β-synthase (2) and methylenetetrahydrofolate reductase (3). An important role in development of hyperhomocysteinemia is also played by deficiency of folic acid, vitamins B 6 and B 12 (4). Hyperhomocysteinemia is defined when plasma homocysteine concentration exceeds l6μmol/l (5). In clinical setting it is useful not only to assess homocysteine level in fasting blood samples, but also to measure it after methionine loading test (6). The mechanism through which hyperhomocysteinemia promotes development of atherosclerosis are not clear. Homocysteine is toxic to vascular endothelium (7), it promotes thrombosis (8) and potentiates the oxidation of low density lipoprotein (LDL) in vitro (9). It has been suggested lately that oxidation of LDL may be one of the main factors involved in initial development of atherosclerotic lesions (10). The aim of our study was to assess the relationship between hyperhomocysteinemia and lipid peroxidation in vivo. The experimental model was the oral methionine loading test.
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