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. Author manuscript; available in PMC: 2017 Dec 1.
Published in final edited form as: Trends Neurosci. 2016 Nov 12;39(12):862–879. doi: 10.1016/j.tins.2016.10.003

Figure 1. Induction of nitroxidative species after tissue injury.

Figure 1

Nitroxidative species can induce posttranslational modifications of proteins and lipids, which subsequently drive pathological pain by modulating nociceptive neurotransmission, activating TRP channels, inducing mitochondrial dysfunction, and induce inflammatory signaling. In healthy cells, endogenous antioxidant systems prevent nitroxidative damage. Cell damage/pathology can perturb this balance, driving accumulation of potentially damaging nitroxidative species. O2: oxygen; NO: nitric oxide; O2•−: superoxide; ONOO−: peroxynitrite; H2O2: hydrogen peroxide; •OH: hydroxyl radical; H2O: water; NOX: NADPH oxidase; NOS: nitric oxide synathse; mETC: mitochondrial electron transport chain; SOD: superoxide dismutase; CAT: catalase; GPx: glutathione; HO: heme oxygenase.