Protective roles of ascorbic acid in oxidative stress induced by depletion of superoxide dismutase in vertebrate cells
Autor: | Hanako Yoshii, Masayuki Seki, Masami Watanabe, Akari Yoshimura, Hisakatsu Nawata, Genro Kashino, Takemi Enomoto, Yuki Tamari, Keizo Tano, Eri Inoue |
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Rok vydání: | 2012 |
Předmět: |
antioxidant
Antioxidant Mitochondrial intermembrane space medicine.medical_treatment SOD1 SOD2 Ascorbic Acid medicine.disease_cause Biochemistry Antioxidants Superoxide dismutase Gene Knockout Techniques chemistry.chemical_compound Superoxide Dismutase-1 medicine Animals Humans skin and connective tissue diseases biology Superoxide Dismutase Superoxide DT40 conditional knockout cell nutritional and metabolic diseases General Medicine Ascorbic acid Mitochondria Oxidative Stress chemistry Vertebrates cardiovascular system biology.protein Reactive Oxygen Species Chickens Oxidative stress |
Zdroj: | Free Radical Research. 47:1-7 |
ISSN: | 1029-2470 1071-5762 |
DOI: | 10.3109/10715762.2012.734916 |
Popis: | Superoxide dismutases (SODs) are antioxidant proteins that convert superoxide to hydrogen peroxide. In vertebrate cells, SOD1 is mainly present in the cytoplasm, with small levels also found in the nucleus and mitochondrial intermembrane space, and SOD2 is present in the mitochondrial matrix. Previously, the authors conditionally disrupted the SOD1 or SOD2 gene in DT40 cells and found that depletion of SOD1 caused lethality, while depletion of SOD2 led to growth retardation. The observations from previous work showed that the lethality observed in SOD1-depleted cells was completely rescued by ascorbic acid. Ascorbic acid is a water-soluble antioxidant present in biological fluids; however, the exact target for its antioxidant effects is not known. In this study, the authors demonstrated that ascorbic acid offset growth defects observed in SOD2-depleted cells and also lowered mitochondrial superoxide to physiological levels in both SOD1- or SOD2-depleted cells. Moreover, depletion of SOD1 or SOD2 resulted in the accumulation of intracellular oxidative stress, and this increased oxidative stress was reduced by ascorbic acid. Taken together, this study suggests that ascorbic acid can be applied as a nontoxic antioxidant that mimics the functions of cytoplasmic and mitochondrial SODs. |
Databáze: | OpenAIRE |
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