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2018;44(Suppl 2):S4049

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

The prodrug design strategy involves modifying the active drug molecule into a non-toxic form, which is then activated and released upon reaching the target site [5,6,7]

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