Fructose autoxidation produces hydroxyl radical and glyoxal that damage biomolecules.

摘要

Background. Fructose is one of the most commonly used sweeteners in food industry and large consumption of it has been blamed for marked increase in obese population. Also, high fructose diet has not only induced insulin resistance syndrome that comprises obesity, hypertension, and glucose intolerance but also caused oxidative damage to protein in rodents. Hypothesis. Based upon its chemical structure, fructose may have higher oxidative potential than glucose, resulting in formation of more free radical and dicarbonyl than glucose. Goals. Fructose has been studied regarding its free radical and dicarbonyl formation in comparison to common dietary mono saccharides, glucose, galactose, ribose and the most reactive triose, glyceraldehyde. Method. Five sugars, glucose, galactose, fructose, ribose, and glyceraldehyde were separately incubated in pH 7.4 phosphate buffer at 37°C in the presence or absence of L-lysine for 18 days. All the reaction vessels contain 10 muM FeSO4 as a catalyst for autoxidation of monosaccharide. A portion of reaction mixture was collected every third day for HPLC assay of hydroxyl radical reaction with salicylic acid and dicarbonyl reaction with Girard-T reagent. Result. In the absence of amino acid, glyceraldehyde generated the highest amounts of hydroxyl radical. Next was fructose and ribose that showed marginal difference in hydroxyl radical generation. (Abstract shortened by UMI.)