ABSTRACT
Oxidative stress is widely believed to play a central role in the pathogenesis of late diabetic complications. Recently, the understanding of oxidative stress in diabetes has been improved by the availability of assays exactly determining defined products of reactive oxygen species. These studies have revealed oxi dative stress to occur before diabetic complications are present, further sup porting the concept that oxidative stress is pivotal for the development of diabetic complications. Studies looking at the oxidative stress-activated tran scription factor NF-κΒ help to understand the cellular consequences of oxida tive stress at the molecular level. However, the occurrence of oxidative stress and oxygen species-mediated secondary end products are not sufficient proof for the hypothesis of oxidative stress-dependent diabetic complications. It has to be demonstrated that antioxidant therapy does not only reduce plasmatic markers of oxidative stress and subsequent NF-κΒ activation but also late diabetic complications.
