Anesthesiology and Apoptosis

Abstract

Necrosis is, in general, an unnatural cell death that rapidly occurs in response to severe insults such as poisons, anoxia, infections and trauma. Apoptosis or programmed cell death, unlike necrosis, is a physiological cell death that causes cell deletion without inflammation, release of cellular contents. In apoptosis, individual cells separate from their neighbors and begin a characteristic sequence of structural and biological changes. These changes include cell shrinkage, condensation of chromatin, DNA degradation, activation of caspase cascade. Finally, the cell itself fragments to form apoptotic bodies that engulfed by nearby phagocytes. Apoptosis is distinguished from necrosis in that gene activation is a prominent mechanism regulating cell survival. It is an essential physiological process that plays a critical role in development and tissue homeostasis and cell population control. However, apoptosis plays an important role in the pathogenesis of a number of disease. In the anesthesiology, apoptosis may contribute to major organ damage associated with ischemic/reperfusion injury, it has long been considered to represent necrosis. Apoptosis remains the important clinical consequence of ischemic/reperfusion injury. Free radicals, tumor necrosis factor-a (TNF-alpha), protein kinase c (PKC), caspases, P53, bcl-2 family and calcium have been suggested and frequently cited as important mediators for apoptosis. In this review, I will describe the known mediators and mechanism underlying apoptosis in major organ exposed to ischemic/reperfusion injury, because the usefulness and effectiveness of any therapeutic interventions for cell deaths after ischemic/reperfusion injury depends on a clear understanding of mechanism of apoptosis.