EFFECT OF CHEMICAL ANOXIA ON PROTEIN-KINASE-C AND NA+ K+-ATPASE IN HEPATOCYTES OF GOLDFISH (CARASSIUS-AURATUS) AND RAINBOW-TROUT (ONCORHYNCHUS-MYKISS)/

Protein kinase C (PKC) and Na+/K+-ATPase in hepatocytes from the anoxi a-tolerant goldfish (Carassius auratus) and the anoxia-intolerant rain bow trout (Oncorhynchus mykiss) were studied to determine their role i n the anoxic response of these cells. PKC and Na+/K+-ATPase activities were measured for up to 90 min in the absence (normoxia) and presence (chemical anoxia) of 2 mmol l(-1) sodium cyanide. PKC activity of nor moxic cells from both species remained constant for the entire experim ental period, Addition of cyanide had no effect on PKC activity of tro ut cells, which was maintained at 25% of maximal PKC activity. In gold fish hepatocytes, PKC activity remained constant at 56% of maximal PKC activity for 30 min but fell to 27% after 90 min of anoxic exposure. ATPase activity was measured in hepatocytes exposed to 100 nmol l(-1) phorbol-12,13-dibutyrate (PdBu), a treatment which enhanced PKC activi ty to its maximum level, In trout cells, there was no significant chan ge in Na+/K+-ATPase activity whereas in goldfish hepatocytes a signifi cant increase to about 150% of the respective controls was observed. O n the basis of the experimental evidence that in hepatocytes of goldfi sh (1) PKC and Na+/K+-ATPase activities decreased in parallel during c hemical anoxia and (2) a stimulation of PKC activity by PdBu increased Na+/K+-ATPase activity, we postulate that PKC activity in goldfish, b ut not in trout, may be implicated in the Na+/K+-ATPase inhibition obs erved under anoxia.