Oxidative stress also participates in the CIS-mediated neuropathy through a dysregulation of the products of lipid peroxidation (thiobarbituric acid reactive substance (TBARS) or 4-hydroxy-2-nonenal (4-HNE)) and Nrf2 transcription factor levels, which protect against the free radical injury by regulating antioxidant enzymes, for example heme oxygenase-1 (HO-1), superoxide dismutase-1 (SOD-1) and catalase [26]. Here, SOD1 is linked to in situ carcinoma.