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An accumulation of excess intracellular oxidants can promote redox-mediated signaling events, including antioxidant responses, such as the activation of nuclear factor erythroid 2-related factor 2 (Nrf2) [3], as well as promote the activation of proinflammatory pathways that are mediated by redox-sensitive transcription factors, such as nuclear factor kappa B (NFκB) and activator protein 1 (AP-1) [4–6]

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