Oxidative Stress

Introduction

Reactive oxygen species (ROS) are continuously formed in biological systems. ROS comes in common forms such as Superoxide (O2•−), Hydrogen Peroxide (H2O2), and perhaps the most deleterious, the Hydroxyl Radical (OH•). These free radicals wreak havoc on the cell and lead to protein dysfunction, DNA damage, and lipid peroxidation, resulting in apoptosis. Any increase in radical production or decrease in the defense against ROS induces oxidative stress. This imbalance between ROS formation and ROS detoxification is believed to be involved in a variety of pathogenic processes, such as ischemia-reperfusion (I/R) injury. During the reperfusion phase following ischemia, production of ROS increases remarkably, leading to the breakdown of antioxidant systems and generates rapid and severe damage. Various markers indicating oxidative stress have been used in experimental and clinical studies. Ascorbic Acid is one example of an antioxidant that forms into a radical upon oxidation of a reactive oxygen species like OH• and could be utilized as an in vivo precursor to I/R injury. In vitro analysis of ascorbate via electron paramagnetic resonance (EPR) could suggest a positive correlation between the electron spin resonance (ESR) intensity of the ascorbate free radical and the severity of radical oxygen formation.

Spin Trapping Technique

References

Finkel, T; Holbrook, NJ, Oxidants, oxidative stress and the biology of ageing, Nature, 408, pp 239-247.

[[LLoyd, Roger; Hanna, Phillip; Mason, Ronald, The origin of the hydroxyl radical oxygen in the fenton reaction, Free Radical Biology and Medicine, 22, 5. pp 885-888.]]