ABSTRACT
Diabetes-induced oxidative stress in target tissues for diabetic complications, including peripheral nerve, results from at least three mechanisms (Fig. 1), including glucose autooxidation, formation of advanced glycation end prod ucts, and increased aldose reductase (AR) activity (1). The contribution of oxidative stress to peripheral diabetic neuropathy has been well established (1-6). Diabetes-induced oxidative stress leads to decreased endoneurial blood flow with resulting endoneurial hypoxia (1-4,6,7). Increased formation of re active oxygen species (ROS) impairs neurotrophic support (8) and causes re dox imbalances (9), energy deficiency (9), and perhaps defects in ion-transport mechanisms, which theoretically can be both mediated by and be independent of the corresponding changes in nerve blood flow.
