“…Under homeostatic conditions, Nrf2 influences mitochondrial membrane potential, fatty acid oxidation, the availability of substrates for respiration, as well as ATP synthesis [44]. But under stress conditions, Nrf2 detaches from Keap1 and translocates to the nucleus, and counteracts the promotion of ROS production through transcriptional increase of antioxidant proteins, including SOD, CAT, HO1, NQO1, GCLM and GCLC, which subsequently modulate oxidative stress, apoptosis and inflammation in diverse neurological disorders [45,46]. Previous studies have documented that after SCI, oxidative stress markers specific to lipid and protein oxidation, namely 4-HNE and 3-NT, all up-regulate in the injured tissue homogenates [47,48].…”