The electron transport chain (ETC) has become a promising pharmacological target as ETC impairment by reactive oxygen species (ROS) has been detected in several diseases. Therefore, for a better understanding of the actions of mitochondria-targeted antioxidants, it must be considered the interplay between the sources of ROS during disease, the chemical interconversions of ROS and their differential reactivity with ETC components. This review contrasts these aspects with available data about mitochondrial damage in specific diseases to give an insight into the importance of ROS chemistry in the rational use of mitochondria-targeted antioxidants, putting emphasis on the case of MitoQ.
Keywords: Lipid peroxidation, thiol oxidation, iron, respiratory chain, MitoQ, ischemia-reperfusion, neurodegeneration, liver diseases, electron transport chain, ETC impairment, reactive oxygen species, mitochondrial damage
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