SOD1 and neoplasm: Payent et al., [63] and Lv et al. [15] revealed that mitochondrial ROS exerted dual roles in tumor-suppression or tumor-promotion, and in the presence of a high level of mitROS that will cause tissue damage and cell death, AsA treatment could remarkably inhibit ROS formation and increase the GSH, superoxide dismutase (SOD) and CAT levels to attenuate oxidative stress damage, whereas Park et al. [64] and Li et al. [28] indicated that AsA caused the induction of ROS generation to induce apoptosis in SK-MEL-2 and HepG2 cells.