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

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.

• Authors: G Krumschnabel, M E Frischmann, P J Schwarzbaum, W Wieser
• Journal: Archives of biochemistry and biophysics (Arch Biochem Biophys) Vol. 353 Issue 2 Pg. 199-206 (May 15 1998) ISSN: 0003-9861 [Print] United States
• PMID: 9606953 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Cyanides
• Potassium
• Calcium

Topics

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