Cellular injury, mechanisms

Based upon theoretical considerations of the mechanisms of hypothermic-induced cellular injury, we developed the University of Wisconsin organ preservation solution (UW solution) that has had a widespread and dramatic effect on organ preservation (Table 2). Prior to the development of this solution, the liver and pancreas could be preserved for only four to six hours. Thus, there was a large time constraint on liver and pancreas transplantation and many cadaveric organs were wasted. However, the UW solution increased preservation duration to 48 to 72 hours, and dramatically increased the quality and numbers of these organs transplanted. Furthermore, this solution appears effective for the preservation of the kidney for three days and the heart for at least 15 hours. 

Nordmann, R., Ribiere, C. and Rouach, H. (1992). Implication of free radical mechanisms in ethanol-induced cellular injury. Free Rad. Biol. Med. 12, 219-240. 

Infection 1. Invasion and multiplication of microorganisms in body tissues, which may be clinically unapparent or result in local cellular injury due to competitive metabolism, toxins, intracellular replication, or antigen-antibody response. The infection may remain localized, subclinical, and temporary if the body s defensive mechanisms are effective. A local infection may persist and spread by extension to become an acute, subacute, or chronic clinical infection or disease state. A local infection may also become systemic when the microorganisms gain access to the lymphatic or vascular system. 2. An infectious disease. [EU]... 

These somewhat simplified descriptions of mechanisms that initiate cellular injury, and of the ways in which cells and tissues respond to these injuries will, as noted at the outset, be helpful as we describe various manifestations of toxicity and carcinogenicity. We distinguish between toxic injuries, which are typically seen in animal experiments and are usually described in the terms defined in the foregoing, and the various medical conditions we call diseases. Many toxic responses can lead to disease, but we also consider toxic injuries to be adverse effects, whether or not they are known to lead to specific diseases. 

It now seems that cytosolic calcium may not play a central role in the initiation of oxidative injury as changes in calcium homeostasis occur well after the appearance of other indications of cellular injury. However, mitochondrial lesions do occur early on in the time course of oxidative cellular damage, and calcium may indeed play a role in these. Changes in concentrations of calcium will, however, result in the activation of signaling mechanisms and alterations in cellular structure and in gene expression. Such alterations may in some instances play a critical role in cellular toxicity. For example, increases in cytosolic Ca2+ inhibit mitochondrial function. 

Reed DJ. Mechanisms of chemically induced cell injury and cellular protection mechanisms. In Hodgson E, Smart RC, eds. Introduction to Biochemical Toxicology. 3rd ed. Connecticut Appleton-Lange, 2001. 

Glutathione-Dependent Mechanisms in Chemically Induced Cell Injury and Cellular Protection Mechanisms... 

Ischemic brain injury results in the death of distinct susceptible populations of neurons in the brain. In addition, the injury concurrently triggers cellular repair mechanisms. SVZ precursors can be recruited following transient middle cerebral artery occlusion (Jin et al., 2001 Zhang et al., 2001). In this stroke... 

For non-sparged cultures of non-porous microcarriers, cellular injury is likely to be the result of three distinct mechanisms (Papoutsakis, 1991a) interactions... 

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