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AJP - Regulatory, Integrative and Comparative Physiology, Vol 273, Issue 1 307-R316, Copyright © 1997 by American Physiological Society
ARTICLES |
G. Krumschnabel, P. J. Schwarzbaum, C. Biasi, M. Dorigatti and W. Wieser
Abteilung fur Okophysiologie, Universitat Innsbruck, Austria.
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 Ca2+ indicator fura 2, we observed that both chemical anoxia and true anoxia led to an increase of the concentration of cytosolic free calcium (Ca2+i) in the anoxia-sensitive hepatocytes of rainbow trout, whereas Ca2+i was maintained at control levels in the anoxia-tolerant hepatocytes of goldfish. Various lines of evidence suggest an intracellular origin of the Ca2+ increase observed in trout cells. Cyclosporin A, a specific inhibitor of the mitochondrial permeability transition pore in mammalian cells, was ineffective in preventing the Ca2+ increase, whereas a high dose of fructose depressed the Ca2+ surge by approximately 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 Ca2+i 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 Ca2+i.
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