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However, material properties, such as elastic modulus and stress, do not recover to the same extent during the same time span 20,23,24
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Because this high antioxidant capacity enhances cell survival and impairs cellular responses to anticancer therapy (79), induction of ROS-mediated damage in cancer cells with use of appropriate pharmacological agents that either promote ROS generation beyond the cellular anti-oxidative capacity or disable the cellular antioxidant system, has been considered as a radical therapeutic strategy for preferential targeting of cancer cells (79)
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