Abstract
It is well known that ROS, generated via various enzymatic and non-enzymatic pathways, can cause the damage of biomolecules. Using γ-irradiation and/or Fe2+/t-BuOOH reagent system for •OH and •OR generation we have shown that glucose metabolites and their analogs (fructose-1,6-bisphosphate, glyceraldehyde-3-phosphate, glycerol-1-phosphate etc.) undergo free radical destruction in aqueous solutions. As a result of such reactions inorganic phosphate and carbonyl products were formed. Among free radical transformation products of starting compounds glyoxal and methylglyoxal (MG) have also been found. The mechanisms for such transformations were proposed. It is known that dicarbonyls possess high toxicity, MG is a potent protein glycating agent, MG-derived hydroimidazolone (MG-H1) is often the major advanced glycation end-product in proteins of tissues and body fluids, increasing in diabetes and associated vascular complications, renal failure, cirrhosis, Alzheimer's disease, arthritis, Parkinson's disease and ageing. The obtained data are recommended to consider during estimation of ROS-induced pathophysiological processes involving glucose metabolites.
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