Table 1 |
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Courtesy [9] origins of reactive oxygen species (ROS) which produce redox stress |
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I |
Excess O2 (oxygen therapy) |
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II |
Absorption of radiant energy (ultraviolet light) or ionizing radiation (radiotherapy) |
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III |
Exposure to toxins: carbon tetrachloride, dioxin, alloxan and streptozotocin to name just a few |
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IV |
Reduction-oxidation (redox) reactions during normal physiologic processes (cellular respiration) |
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A. Respiratory chain enzymes and oxygen |
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B. Xanthine oxidase |
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C. Cytochrome P450 monooxygenase activity |
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D. NAD(P)H / NADH oxidase |
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E. Fenton reaction: Fe++ + H2O2 → Fe+++ + OH + OH- |
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F. Haber-Weiss Reaction H2O2 + O2- → -OH- + O2 +OH- |
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V |
Ischemia – Ischemia reperfusion injury |
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VI |
Inflammatory processes. Acute and chronic |
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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] |
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Hayden and Tyagi Cardiovascular Diabetology 2002 1:3 doi:10.1186/1475-2840-1-3 |
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