Glucose and reactive oxygen species

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Abstract
This review aims at presenting new concepts of glucose-induced damage in diabetes via an increased production of oxygen free radicals. Reactive oxygen species modulate various biological functions by stimulating transduction signals, some of which are involved in diabetes pathogenesis and complications. Diabetes is characterized by high glucose concentrations that lead, via several mechanisms (glucose autoxidation, stimulation of the polyol pathway, activation of the reduced form of nicotinamide adenine dinucleotide phosphate oxidase, and production of advanced glycation endproducts), to an increased production of reactive oxygen species. The resulting oxidative stress (the imbalance between reactive oxygen species production and the antioxidant defences) can play a key role in diabetes pathogenesis. Superoxide radicals generated by the reduced form of nicotinamide adenine dinucleotide phosphate oxidase may thus contribute to impaired endothelium-dependent vascular relaxation by the inactivation of nitric oxide, and more generally to vascular dysfunction, thereby contributing to accelerated atherosclerosis in diabetic patients. The increased production of reactive oxygen species induced by hyperglycaemia has also been suggested to be involved in platelet dysfunction, in tissue remodelling (via metalloproteinases), and in redox regulation of glucose transport in skeletal muscle. Beyond the classic treatments for diabetes, new therapeutic strategies involving antioxidants or anti-advanced glycation endproduct molecules are proposed. Future methods could take into account the signalling pathways and genes that are regulated by reactive oxygen species.