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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]