Abstract
Superoxide dismutases (SODs) are antioxidant proteins converting superoxide to hydrogen peroxide. In vertebrate cells, SOD1 is mainly present in the cytoplasm, and small portions in nucleus and mitochondrial inter-membrane space and SOD2 is present in the mitochondrial matrix. Previously we have conditionally disrupted SOD1 or SOD2 gene in DT40 cells, respectively. SOD1 depletion caused lethality, while depletion of SOD2 showed growth defect. Our intriguing observation from previous work is that lethality observed in SOD1-depleted cells is completely rescued in the presence of ascorbic acid. In this study, we confirmed ascorbic acid offset growth defect observed in SOD2 depleted cell and completely normalized increased mitochondrial superoxide levels in either SOD1 or SOD2 depleted cells. Moreover intracellular oxidative stress reflected by increase of either mitochondrial or cytoplasmic superoxide levels was reduced by ascorbic acid treatment. All the data so far in this study suggested ascorbic acid could be antioxidant which is mimic of either cytoplamic or mitochondrial superoxide dismutase.
