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Table 1 Courtesy [9] origins of reactive oxygen species (ROS) which produce redox stress

From: Intimal redox stress: Accelerated atherosclerosis in metabolic syndrome and type 2 diabetes mellitus. Atheroscleropathy

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]