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Table 1 Courtesy [9] origins of reactive oxygen species (ROS) which produce redox stress
| I | Excess O2 (oxygen therapy) |
| II | Absorption of radiant energy (ultraviolet light) or ionizing radiation (radiotherapy) |
| III | Exposure to toxins: carbon tetrachloride, dioxin, alloxan and streptozotocin to name just a few |
| IV | Reduction-oxidation (redox) reactions during normal physiologic processes (cellular respiration) |
| A. Respiratory chain enzymes and oxygen | |
| B. Xanthine oxidase | |
| C. Cytochrome P450 monooxygenase activity | |
| D. NAD(P)H / NADH oxidase | |
| E. Fenton reaction: Fe++ + H2O2 → Fe+++ + OH + OH- | |
| F. Haber-Weiss Reaction H2O2 + O2- → -OH- + O2 +OH- | |
| V | Ischemia – Ischemia reperfusion injury |
| VI | Inflammatory processes. Acute and chronic |
| VII | Once free ROS radicals form, they can react with membrane lipids, proteins and nucleic acid to initiate auto-catalytic reactions (ROS beget ROS) [9] |
