Hydroxyl radical production and autoxidative glycosylation. Glucose autoxidation as the cause of protein damage in the experimental glycation model of diabetes mellitus and ageing.

摘要: Protein exposed to glucose is cleaved, undergoes conformational change and develops fluorescent adducts (‘glycofluorophores’). These changes are presumed result from the covalent attachment of amino groups. We have demonstrated, however, that fragmentation observed dependent upon hydroxyl radicals produced by autoxidation, or some closely related process, antioxidants dissociate structural damage caused exposure protein incorporation monosaccharide into protein. also provided further evidence glycofluorophore formation metal-catalysed oxidative processes associated with ketoaldehyde formation. If experimental glycation an adequate model tissue occurring in diabetes mellitus, then these studies indicate a therapeutic role for antioxidants.