ABSTRACT
There is much evidence that the formation of various markers of oxidative stress are increased in diabetes: In the plasma of diabetic patients the concen trations of lipid hydroperoxides, isoprostanes, malonic dialdehyde, and oxi dized lipoproteins are elevated (1-6). The intracellular levels of antioxidants such as tocopherol and glutathione are reduced, whereas the enzymatic activity of antioxidative acting enzymes is at least partly increased (7-12). Similarly, there are many reports about the consequences of an imbalance between proand antioxidant actions in the cells (“ oxidative stress” ) and the importance of disturbances in the intracellular antioxidant network for the development of vascular complications in hypertensive or hypercholesterolemic patients. Such a pathophysiological link between oxidative stress and vascular compli cations is in line with many experimental observations, with large epidemio logical studies, and to a lesser extent with recent clinical investigations (1322). There is increasing evidence that the generation of reactive oxygen inter mediates is also of major importance for the development of vascular compli cations in diabetes (23-29). However, neither the mechanisms that specifically lead to the generation of reactive oxygen intermediates (ROI) in hyperglyce-
mic states nor the cascade of reactions linking the formation of ROI with the pathophysiological event are well understood.
