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While elevated blood sugar speeds up the hexosamine biosynthesis pathway (HBP), causing kidney damage and the production of advanced glycosylation end products (AGEs) (4, 5)

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The authors conclude that the indicated SOD2 and SOD3 polymorphisms may be genetic risk factors for the susceptibility and progression of vitiligo suggesting the increased activity of SOD isoforms caused by the variant gene polymorphisms may lead to the accumulation of H 2 O 2 in cytoplasmic, mitochondrial and extracellular compartments resulting in melanocyte oxidative damage