Induction of Superoxide Dismutase Activity by Paraquat or Edu in Human Gingival Fibroblasts
Oxygen free radicals mediate cell injury. These radicals are formed as the reduction of molecular oxygen occurs, initially resulting in the formation of superoxide anions (•02-), then H2O2 and finally H2O. The first line of defense against such radicals is the enzyme superoxide dismutase (SOD), which dismutes •02- to H2O2. Subsequent reactions may involve the antioxidant enzymes catalase (CAT) and glutathione peroxidase (GSHPx). The production of •02- by the redox cycling of paraquat may be responsible for the induction or derepression of SOD activity. The purpose of this study was to develop a model using human cells to investigate the effects of pharmacologic agents which might act as inducers of the antioxidant enzymes SOD, CAT and GSHPx. We developed this model in human gingival fibroblasts using paraquat (PQ) as the positive control. One pharmacologic agent, EDU, N-[2-(2-oxo-l-imidazolidinyl) ethyl]-N-phenylurea (Figure 1), was an inducer of SOD and CAT activities in plants. It protected plants against acute and chronic ozone-induced injury,1 and this tolerance was correlated with increased antioxidant enzyme activities.2 We hypothesized that this heterocyclic urea might induce these enzymes in mammalian cells.
KeywordsAntioxidant Enzyme Glutathione Peroxidase Catalase Activity GSHPx Activity Human Gingival Fibroblast
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