Loss of K+ homeostasis in trout hepatocytes during chemical anoxia: a screening study for potential causes and mechanisms

Arch Biochem Biophys. 1998 May 15;353(2):199-206. doi: 10.1006/abbi.1998.0646.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Anaerobiosis
  • Animals
  • Calcium / metabolism
  • Cell Hypoxia
  • Cyanides / poisoning*
  • Glycolysis
  • Homeostasis / drug effects*
  • Liver / drug effects
  • Liver / physiology*
  • Oncorhynchus mykiss
  • Osmolar Concentration
  • Potassium / physiology*

Substances

  • Cyanides
  • Potassium
  • Calcium