Figure 1
The electron transport chain (ETC) and NADPH oxidases (NOX) take up oxygen to generate superoxide. Superoxide is dismutated by MnSOD and Cu-ZnSOD to generate H2O2. Oxidation of cysteine residues of peroxiredoxin (PRDX) and thioredoxin (TXN) proteins converts H2O2 to water. H2O2 is also converted to water by the glutathione peroxidase-glutathione reductase (GPX-GSR). In the presence of Fe2+ ions, H2O2 is converted to hydroxyl radicals (•OH) via the Fenton reaction. H2O2 and •OH radicals oxidize macromolecules, altering cellular signaling and oxidatively damaging DNA. This leads to gene mutations. The •OH radicals start lipid oxidation of alkyl (R•) groups, which are oxidized to alkoxyl (RO•) and peroxyl (ROO•) radicals. The dotted blue arrows show the source of ROS while purple numbers show the half-life of these radicals (in seconds). Adapted from Purohit et al., 2019 [1].
The fate of ROS

The electron transport chain (ETC) and NADPH oxidases (NOX) take up oxygen to generate superoxide. Superoxide is dismutated by MnSOD and Cu-ZnSOD to generate H2O2. Oxidation of cysteine residues of peroxiredoxin (PRDX) and thioredoxin (TXN) proteins converts H2O2 to water. H2O2 is also converted to water by the glutathione peroxidase-glutathione reductase (GPX-GSR). In the presence of Fe2+ ions, H2O2 is converted to hydroxyl radicals (OH) via the Fenton reaction. H2O2 and OH radicals oxidize macromolecules, altering cellular signaling and oxidatively damaging DNA. This leads to gene mutations. The OH radicals start lipid oxidation of alkyl (R) groups, which are oxidized to alkoxyl (RO) and peroxyl (ROO) radicals. The dotted blue arrows show the source of ROS while purple numbers show the half-life of these radicals (in seconds). Adapted from Purohit et al., 2019 [1].

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