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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)
However, futile quinone redox cycling can lead to a cascade of ROS formation and as such, the link between toxicity and quinone redox cycling is widely acknowledged 5
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Langmuir 26 , 1167011679 (2010)
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