Oxidative Stress
Introduction
Coronary Heart Disease (CHD) is the major mortality cause in the Western Hemisphere. Reinstituting blood flow in the acutely occluded coronary vessel became the standard intervention to prevent Myocardial Infarct (MI) progression. Ever since their conception, thrombolysis, Percutaneous Coronary Intervention (PCI) and Coronary Artery Bypass Grafting (CABG) have been at the forefront of CHD treatment, thus limiting MI size. However, it quickly became apparent that after a period of ischemia, reperfusion itself sets off a cascade of events leading to cell injury. It seems that cellular changes in the ischemic period, prime the cell for a loss of homeostasis once blood flow returns. Generation of reactive oxygen species (ROS) has been found to be the main culprit in both ischemia and reperfusion. Still, the cellular and molecular mechanisms behind this are far from being completely elucidated. Novel insight about this interplay and details about the extent by which each of these players contributes to ischemic-reperfusion injury may allow scientists to devise and design proper interventions that ultimately reduce I/R injury in clinical practice. This article explores the mechanisms behind reactive oxygen species production and possible relevant inhibitors in order to mitigate the effects of ischemia and reperfusion.
References
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.