The oxygen-dependence of cellular energetics was investigated in hepatocytes from goldfish Carassius auratus (anoxia-tolerant) and rainbow trout Oncorhynchus mykiss

found to be independent of O2 concentration over a wide range (Wilson et al., 1979, 1988). Recently, however, Schumacker et al. (1993) and Chandel et al. (1997) reported a marked O2dependence of respiration in rat hepatocytes when hypoxia was maintained over several hours, an experimental approach not applied in previous studies. Furthermore, O2-dependence even under acute hypoxia has been described in chick cardiac myocytes (Budinger et al., 1996). As pointed out by these authors, such a metabolic behaviour might represent an adaptive response to limited O2 supply by slowing down the rate of O2 depletion and thus delaying the onset of anoxia. In a number of recent studies, the hepatocyte of the goldfish Carassius auratus has been characterized as highly tolerant to environmental anoxia, this tolerance being based on the capacity to shut down ATP-consuming functions in synchrony with ATP-producing pathways (Krumschnabel et al., 1994b, 1996, 1997). Considering the above report on anoxia-intolerant rat hepatocytes, the question arises as to whether a similar ability to suppress metabolic activity can also be found at low, as opposed to zero, levels of O2 availability in goldfish hepatocytes. Moreover, the fact that O2-conforming behaviour in chick cardiac myocytes could be elicited during a considerably shorter period of hypoxic exposure (approximately 2 min) than in rat hepatocytes (>2 h) may be related to the generally greater hypoxia-tolerance of cardiac tissue (Arai et al., 1991). Therefore, we hypothesize that, in goldfish hepatocytes, the O2-dependence of respiration, if present, should also be more readily observable than in anoxiaintolerant cells. We addressed this problem by comparing the O2dependence of the energetics of hepatocytes from goldfish and trout Oncorhynchus mykiss, the latter being well characterized as a model for anoxia-intolerant cells (Krumschnabel et al., 1996, 1997; Schwarzbaum et al., 1996). Respiratory rates were determined in cells that were exposed to normoxic or hypoxic conditions either acutely or for 1 h before measurements. Other variables evaluated were the cellular ATP pool, as a measure 951 The Journal of Experimental Biology 203, 951–959 (2000) Printed in Great Britain © The Company of Biologists Limited 2000 JEB2614