ABSTRACT
Patients with non-insulin-dependent diabetes mellitus (NIDDM) are at in creased risk of developing vascular and other complications. This excess risk is only partially explained by the traditional risk factors, including smoking, hypertension, and dyslipidemia (1-3). Therefore, oxidative stress has been proposed as a possible explanation for the accelerated complications in NIDDM (4-7). A major hypothesis is that low-density lipoprotein (LDL) modification by oxidation or glycosylation contributes to tissue damage through cytotoxic reactions with endothelial cells or through further reactions to generate “ modified” LDL that is selectively accumulated by “ scavenger” receptors (8).
