Krumschnabel 1998 Arch Biochem Biophys

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Krumschnabel G, Frischmann ME, Schwarzbaum PJ, Wieser W (1998) Loss of K+ homeostasis in trout hepatocytes during chemical anoxia: a screening study for potential causes and mechanisms. Arch Biochem Biophys 353: 199-206.

» PMID: 9606953

Krumschnabel G, Frischmann ME, Schwarzbaum PJ, Wieser W (1998) Arch Biochem Biophys

Abstract: In isolated trout hepatocytes intoxication with CN- (chemical anoxia) leads to a rapid breakdown of K+ homeostasis. In the present study an attempt has been made to identify the causes and mechanisms underlying this phenomenon. Our results indicate that neither Ca2+ elevation nor cell swelling, both of which occurred during chemical anoxia and could be prevented by exposure to Ca2+ chelating agents or to hyperosmotic conditions, respectively, is solely responsible for the breakdown of K+ homeostasis. From a number of inhibitors of dissipative K+ fluxes tested, only BaCl2, an inhibitor of voltage-gated K+ channels, proved to be effective in significantly reducing K+ efflux during chemical anoxia. The KCl cotransporter known to be involved in regulatory volume decrease after hypoosmotic shock does not seem to be activated during CN(-)-induced cell swelling.

Keywords: Oncorhynchus mykiss, Calcium, Cell swelling, Conductive K+ movement, Glycolysis