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

ELT, M. V. P. N. MUT, G. AMODEO, G. KRUMSCHNABEL, AND P. J. SCHWARZBAUM

JOURNAL OF EXPERIMENTAL BIOLOGY

COMPANY OF BIOLOGISTS LTD

Lugar: Londres; Año: 2003 vol. 206 p. 513 - 522

0022-0949

The relationship between cell volume and K+transmembrane fluxes of goldfish (Carassius auratus)hepatocytes exposed to anisotonic conditions or energeticlimitation was studied and compared with the response ofhepatocytes from trout (Oncorhynchus mykiss) and rat(Rattus rattus). Cell volume was studied by video- andfluorescence microscopy, while K+ fluxes were assessed bymeasuring unidirectional 86Rb+ fluxes.In trout and rat hepatocytes, hyposmotic(180 mosmol l–1) exposure at pH 7.45 caused cell swellingfollowed by a regulatory volume decrease (RVD), aresponse reported to be mediated by net efflux of KCland osmotically obliged water. By contrast, goldfishhepatocytes swelled but showed no RVD under theseconditions. Although in goldfish hepatocytes a net(86Rb+)K+ efflux could be activated by N-ethylmaleimide,this flux was not, or only partially, activated byhyposmotic swelling (120–180 mosmol l–1).Blockage of glycolysis by iodoacetic acid (IAA) did notalter cell volume in goldfish hepatocytes, whereas in thepresence of cyanide (CN–), an inhibitor of oxidativephosphorylation, or CN– plus IAA (CN–+IAA), cellvolume decreased by 3–7%. Although in goldfishhepatocytes, 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 notsignificantly altered by IAA alone. Intracellular K+ lossafter 20 min of exposure to CN– and CN–+IAA amountedto only 3% of the total intracellular K+.Collectively, these observations suggest that goldfishhepatocytes, unlike hepatocytes of anoxia-intolerantspecies, avoid a decoupling of transmembrane K+ fluxes inresponse to an osmotic challenge. This may underlie boththe inability of swollen cells to undergo RVD but alsothe capability of anoxic cells to maintain intracellularK+ concentrations that are almost unaltered, therebyprolonging cell survival.