THE ROLE OF THE MITOCHONDRION IN TRAUMA AND SHOCK

Publisher Website
Google Scholar
Abstract
The mitochondrion of the eukaryotic cell is well known as a “power plant” whose energy is made available via the high-energy phosphate bonds of ATP. This indispensable and superbly adapted organelle appears to have originated as an endosymbiotic bacterium rather than as a eukaryotic creation per se. However, under the dangerous conditions of trauma and shock, the mitochondrion can become destabilized and harm its host cell in a variety of ways. These contrary traits may be, in part, vestiges from the bacterial origins of mitochondria. The mitochondrion can respond to the stress of trauma and shock by opening pores that leak contents into the host cell’s cytoplasm, an event that can trigger programmed cell death or necrosis. In addition, the enormous oxygen consumption by mitochondria presents a two-edged sword in that a deranged mitochondrion can produce reactive oxygen species that damage genes and gene products, inflicting considerable harm to the mitochondrion and its host cell. However, although trauma and shock can cause the mitochondrion to wreak havoc in many ways, an adjuvant intervention with exogenous ATP-MgCl2 after trauma and shock appears useful for reducing cell and organ damage under those conditions.