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To date, it has been observed that the treatment with this kind of antitumor agents causes ROS generation, mitochondrial dysfunction (including frataxin deficiency, mitochondrial DNA damage and defective components of ETC), loss in antioxidant enzymes, ion channels disturbances and nerve tissue damage (protein carbonylation and lipid peroxidation) (Areti et al., in vitro and in vivo biochemical effects after exposure to high concentrations of oxaliplatin, including neuronal activation of the purinoreceptor subtype 7, ROS and NO production, lipid peroxidation, loss of mitochondrial transmembrane potential and further apoptosis via caspase 3 activation