Effect of chemical anoxia on Protein Kinase C and Na,K-ATPase in isolated hepatocytes of goldfish (Carassius auratus) and the rainbow trout (Oncorhynchus mykiss)

SCHWARZBAUM PJ, BERNABEU R, KRUMSCHNABEL G, BIASI CH, WIESER W

JOURNAL OF EXPERIMENTAL BIOLOGY

COMPANY OF BIOLOGISTS LTD

Año: 1996 p. 1515 - 1521

0022-0949

Protein kinase C (PKC) and Na+/K+-ATPase inhepatocytes from the anoxia-tolerant goldfish (Carassiusauratus) and the anoxia-intolerant rainbow trout(Oncorhynchus mykiss) were studied to determine their rolein the anoxic response of these cells. PKC and Na+/K+-ATPase activities were measured for up to 90 min in theabsence (normoxia) and presence (chemical anoxia) of2mmoll-1 sodium cyanide. PKC activity of normoxic cellsfrom both species remained constant for the entireexperimental period. Addition of cyanide had no effect onPKC activity of trout cells, which was maintained at 25%of maximal PKC activity. In goldfish hepatocytes, PKCactivity remained constant at 56% of maximal PKCactivity for 30 min but fell to 27 % after 90 min of anoxicexposure.ATPase activity was measured in hepatocytes exposed to100 nmol l-1 phorbol-12,13-dibutyrate (PdBu), a treatmentwhich enhanced PKC activity to its maximum level. Introut cells, there was no significant change in Na+/K+-ATPase activity whereas in goldfish hepatocytes asignificant increase to about 150 % of the respectivecontrols was observed.On the basis of the experimental evidence that inhepatocytes of goldfish (1) PKC and Na+/K+-ATPaseactivities decreased in parallel during chemical anoxia and(2) a stimulation of PKC activity by PdBu increasedNa+/K+-ATPase activity, we postulate that PKC activity ingoldfish, but not in trout, may be implicated in the Na+/K+-ATPase inhibition observed under anoxia.