Enhanced Susceptibility to Oxidation and Diminished Vitamin E Content of LDL from Patients with Stable Coronary Artery Disease (Lipids, Lipoproteins, And Cardiovascular Risk Factors‪)‬

In vitro and animal model studies provide an ever-increasing body of evidence that oxidation of LDL or related oxidative mechanisms play a major role in atherogenesis (1). Oxidative modification of LDL confers several properties to LDL that render the particle atherogenic. Oxidized LDL induces the transformation of macrophages into foam cells; in addition, it is cytotoxic and immunogenic and may have vasoconstrictor and prothrombotic effects (2, 3). The evaluation of LDL oxidation in vivo is difficult. One of the main problems is that LDL oxidation is likely to occur in the intima of the artery wall rather than in the general circulation (4). Even if some lipoproteins are oxidized in the circulation, the concentrations of these modified lipoproteins may be difficult to detect and may not reflect the extent of oxidation occurring in the arterial wall. Thus, susceptibility of LDL to in vitro oxidation has been proposed as an indicator of the response of LDL to in vivo oxidative stress. Much information relating to oxidized LDL has been acquired from studies focusing on various animals. However, the role of LDL susceptibility to oxidation as a risk factor for coronary artery disease (CAD)[5] in humans has not been fully explored. Divergent information is available in this field, which may be explained in part by the use by investigators of small sample sizes (5-8) or nonspecific methods for evaluation of susceptibility of LDL to oxidation (9). Quantitatively, vitamin E is the major antioxidant in LDL and is generally considered to protect LDL against oxidation (10). However, conflicting results were also reported concerning the role of vitamin E in atherosclerosis (11). Recently, one interventional study showed a null effect of vitamin E on atherosclerosis (12). Moreover, a recent in vitro study has shown that vitamin E can be prooxidative rather than protective for lipids in isolated LDL (13).