Peroxiredoxin V Protects against UVB-Induced Damage of Keratinocytes

Ultraviolet B (UVB) irradiation generates reactive oxygen species (ROS), which can damage exposed skin cells. Mitochondria and NADPH oxidase are the two principal producers of ROS in UVB-irradiated keratinocytes. Peroxiredoxin V (PrxV) is a mitochondrial cytosolic cysteine-dependent peroxidase enzyme that robustly removes H2O2. We investigated PrxV’s role protecting epidermal keratinocytes against UVB-induced damage. separated H2O2 levels from other types using fluorescent indicators. Upon UVB irradiation, PrxV-knockdown HaCaT human showed higher than PrxV-expressing controls. PrxV depletion enhanced hyperoxidation-mediated inactivation PrxIII PrxI PrxII PrxV-depleted exhibited dysfunction were more susceptible to apoptosis through decreased consumption rate, loss membrane potential, cardiolipin oxidation, cytochrome C release, caspase activation. Our findings show serves protect such as apoptosis, not only by directly removing but also indirectly improving catalytic activity PrxII. It possible strengthening defenses could aid preventing