Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology
ReviewNecrotic volume increase and the early physiology of necrosis☆
Section snippets
To apoptose or to necrose?
Whether cells die by apoptosis or by necrosis can have profound implications for local homeostasis and this has much to do with tissue inflammation. Necrosis is pro-inflammatory, while apoptosis is anti-inflammatory. A mechanism to explain this contrast was suggested by the observation that necrotic cells and apoptotic cells elicit opposite effects on the cytotoxic and phagocitic activities of tissue macrophages (Voll et al., 1997, Fadok et al., 1998, Melcher et al., 1998). The
Early ionic events in cell death
Necrotic cell death is characterised by a relatively stereotyped sequence of events. Regardless of the primary insult, e.g. anoxia, metabolic inhibitors, free radicals, etc, ATP levels (or more critically [ATP]i/[ADP]i) drop to near zero in the matter of seconds. In anoxia or chemical hypoxia, energy depletion is adequately explained by defective ATP production in the face of continued ATP hydrolysis by ion pumps, protein synthesis and degradation, etc. In free radical-induced necrosis, the
Ion channels as effectors of cell death
In stressed cells, passive inhibition of the Na+/K+ pump have long been thought to play a major role in the intracellular accumulation of Na+ (Cotran et al., 1999). However, recent data from several laboratories are in conflict with such hypothesis. For example, the rate of accumulation elicited by menadione or KCN was 10-fold higher than that evoked by the pump blocker ouabain (Carini et al., 1999). In endothelial cells, exposure to tert-butyl hydroperoxide not only failed to inhibit but
Positive feedbacks and negative cross-talk in early cell death
Several positive feedback loops that close during early cell injury make of NVI a highly regenerative phenomenon. Upon activation of NSCCs by free-radicals or low [ATP]i, high [Na+]i will activate the Na+/K+ pump, which will in turn decrease cell ATP and further activate NSCCs. NSCC, by a mechanism that is not yet clear, can cause a massive increase in cytosolic Ca2+ (Fig. 1). High calcium will perpetuate ATP depletion by several mechanisms including Ca2+-ATPase activation, further NSCC
Acknowledgements
We thank Claudio Hetz for helpful discussions. This work was supported by Fondecyt 1990782. Institutional support to the Centro de Estudios Cientı́ficos (CECS) from Fuerza Aérea de Chile, I. Municipalidad de Las Condes and a group of chilean private companies (AFP Provida, CODELCO, Empresas CMPC, Telefónica del Sur y Masisa S.A.) is also acknowledged. We thank support obtained through the International Program of the Howard Hughes Medical Institute and Cátedra Presidencial en Ciencias (to
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This paper was originally presented at a symposium dedicated to the memory of Marcel Florkin, held within the ESCPB 21st International Congress, Liège, Belgium, July 24–28, 2000.