Fig. 2.

Oxidative stress-related biomarkers in the brain. The mitochondrion is considered to be the major intracellular production house of ROS. Several enzymes, such as NOX, XO, and uncoupled form of NOS can trigger O₂^•− production. NOS also catalyze the metabolic reaction of amino acid to produce NO. NO reacts with O₂^•− and produces ONOO^•−, a RNS. O₂^•− is converted into H₂O₂ by the action of SOD, which subsequently produces OH^•−. H₂O₂ also yields HOCl by the action of MPO, which again yields O₂^•− and highly active Cl⁻. These highly active free radicals deplete GSH and endorse oxidative damages to cellular lipids, proteins, and DNA, resulting in aberrant levels of some specific biochemical markers in the blood circulation. Thus, these specific biochemical markers could serve as potential OS-related biomarkers. Red arrows indicate downstream events and red lines indicate inhibition. 4-HNE, 4-hydroxynonenal; 8-iso-PGF2α, 8-Epi-prostaglandin F2alpha; 8-OHdG, 8-hydroxydeoxyguanosine; DNA, deoxyribonucleic acid; H₂O₂, hydrogen peroxide; HOCl, hypochlorous acid; Keap1, Kelch-like ECH-associated protein 1; MDA, malondialdehyde; MPO, myeloperoxidase; NO, nitric oxide; NOS, nitric oxide synthase; NOX, NADPH oxidase; Nrf-2, nuclear factor erythroid 2-related factor 2; O₂^•−, superoxide; OH^•−, hydroxyl radical; ONOO^•−, peroxynitrite; ROS, reactive oxygen species; SOD, superoxide dismutase; TBARS, thiobarbituric acid reactive substances; XO, xanthine oxidase