Volumetric and ionic responses of goldfish hepatocytes to anisotonic exposure and energetic limitation

• Published in: Journal of Experimental Biology
• Main Authors: Espelt, M. V., Mut, P. N., Amodeo, G., Krumschnabel, G., Schwarzbaum, P. J.
• Format: Text
• Language: English
• Published: Company of Biologists 2003
• Subjects: Research Article; Rattus rattus
• Online Access: http://jeb.biologists.org/cgi/content/short/206/3/513; https://doi.org/10.1242/jeb.00117

The relationship between cell volume and K+ transmembrane fluxes of goldfish ( Carassius auratus ) hepatocytes exposed to anisotonic conditions or energetic limitation was studied and compared with the response of hepatocytes from trout ( Oncorhynchus mykiss ) and rat ( Rattus rattus ). Cell volume was studied by video- and fluorescence microscopy, while K+ fluxes were assessed by measuring unidirectional 86Rb+ fluxes. In trout and rat hepatocytes, hyposmotic (180 mosmoll-1) exposure at pH 7.45 caused cell swelling followed by a regulatory volume decrease (RVD), a response reported to be mediated by net efflux of KCl and osmotically obliged water. By contrast, goldfish hepatocytes swelled but showed no RVD under these conditions. Although in goldfish hepatocytes a net (86Rb+)K+ efflux could be activated by N -ethylmaleimide, this flux was not, or only partially, activated by hyposmotic swelling (120-180 mosmoll-1). Blockage of glycolysis by iodoacetic acid (IAA) did not alter cell volume in goldfish hepatocytes, whereas in the presence of cyanide (CN-), an inhibitor of oxidative phosphorylation, or CN- plus IAA (CN-+IAA), cell volume decreased by 3-7%. Although in goldfish hepatocytes, energetic limitation had no effect on (86Rb+)K+ efflux, (86Rb+)K+ influx decreased by 57-66% in the presence of CN- and CN-+IAA but was not significantly altered by IAA alone. Intracellular K+ loss after 20 min of exposure to CN- and CN-+IAA amounted to only 3% of the total intracellular K+. Collectively, these observations suggest that goldfish hepatocytes, unlike hepatocytes of anoxia-intolerant species, avoid a decoupling of transmembrane K+ fluxes in response to an osmotic challenge. This may underlie both the inability of swollen cells to undergo RVD but also the capability of anoxic cells to maintain intracellular K+ concentrations that are almost unaltered, thereby prolonging cell survival.