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Biol. Res ; 35(2): 215-222, 2002. graf
Article in English | LILACS | ID: lil-323344

ABSTRACT

Necrosis is considered as a non-specific form of cell death that induces tissue inflammation and is preceded by cell swelling. This increase in cell volume has been ascribed mainly to defective outward pumping of Na+ caused by metabolic depletion and/or to increased Na+ influx via membrane transporters. A specific mechanism of swelling and necrosis driven by the influx of Na+ through nonselective cation channels has been recently proposed (Barros et al., 2001a). We have characterized further the properties of the nonselective cation channel (NSCC) in HTC cells. The NSCC shows a conductance of approximately 18 pS, is equally permeable to Na+ and K+, impermeant to Ca2+, requires high intracellular Ca2+ as well as low intracellular ATP for activation and is inhibited by flufenamic acid. Hydrogen peroxide induced a significant increase in cell volume that was dependent on external Na+. We propose that the NSCC, which is ubiquitous though largely inactive in healthy cells, becomes activated under severe oxidative stress. The ensuing Na+ influx initiates via positive feedback a series of metabolic and electrolytic disturbances, resulting in cell death by necrosis


Subject(s)
Animals , Rats , Carcinoma, Hepatocellular , Ion Channels , Liver Neoplasms , Oxidative Stress , Adenosine Triphosphate , Anti-Inflammatory Agents, Non-Steroidal , Cell Death , Cell Size , Flufenamic Acid , Hydrogen Peroxide , Ion Channels , Oxidants , Sodium , Tumor Cells, Cultured
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