Effects of energy limitation on Ca2+ and K+ homeostasis in anoxia-tolerant and anoxia-intolerant hepatocytes
Krumschnabel, G.; Schwarzbaum, P.J.; Biasi, C.; Dorigatti, M.; Wieser, W.
American Journal of Physiology 273(1 Pt 2): R307-R316
1997
ISSN/ISBN: 0002-9513 PMID: 9249565 Document Number: 482391
To gain more insight into the mechanistic basis of anoxia tolerance and intolerance, a comparative study was conducted on calcium homeostasis in goldfish and trout hepatocytes subjected to different forms of energy limitation. Using the fluorescent Ca-2+ indicator fura 2, we observed that both chemical anoxia and true anoxia led to an increase of the concentration of cytosolic free calcium (Ca-i-2+) in the anoxia-sensitive hepatocytes of rainbow trout, whereas Ca-i-2+ was maintained at control levels in the anoxia-tolerant hepatocytes of goldfish. Various lines of evidence suggest an intracellular origin of the Ca-2+ increase observed in trout cells. Cyclosporin A, a specific inhibitor of the mitochondrial permeability transition pore in mammalian cells, was ineffective in preventing the Ca-2+ increase, whereas a high dose of fructose depressed the Ca-2+ surge by apprx 50%. The latter effect was not accompanied by improvement of the energetic state of the cells. A comparison of chemical anoxia with true (physiological) anoxia revealed that both treatments affected energy metabolism to a similar degree in trout hepatocytes, whereas the decrease of ATP seen in goldfish hepatocytes during chemical anoxia was absent during true anoxia. Elevation of Ca-i-2+ with the calcium ionophore A-23187 led to a decoupling of unidirectional K+ fluxes in both normoxic and anoxic trout cells, whereas in goldfish hepatocytes the coupling of K+ fluxes was not affected by the rise of Ca-i-2+.