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]

Hayden and Tyagi Cardiovascular Diabetology 2002 1:3   doi:10.1186/1475-2840-1-3