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Furthermore, the transition between reduced and oxidized forms of non-enzymatic antioxidants also plays a role in determining the outcome of ferroptotic cell death [217, 218]

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Therapeutics based on mitochondrial dysfunction and oxidative stress, such as mitochondria-targeted antioxidant [10-(4,5-dimethoxy-2-methyl-3,6-dioxo-1,4-cyclohexadien-1-yl)decyl]triphenylphosphonium methanesulfonate (MitoQ), modify disease progression by slowing the decline of mitochondrial function and disease progression in the SOD1 G93A mouse model of ALS (Miquel et al., 2014)

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