Abstract
Energy production in rat liver slices exposed to anaerobiosis is of insufficient magnitude to maintain active cation transport. It was hypothesized that electron-accepting metabolites could facilitate electron flow under anaerobiosis thereby stimulating mitochondrial and glycolytic ATP production. Rat liver slices were subjected to the following protocol: 80 min. at 0-1 C in Krebs-Ringer bicarbonate, 95% O2, 5% CO2; addition of experimental or control solution to the incubation flask; gas changed to 95% O2, 5% CO2; flasks maintained at 0.1 C for an additional 10 min.; and incubation continued at 37 C for 1 hr. A comparable ability to reaccumulate K+ and extrude Na+ occurred in oxygenated tissues and in anaerobic slices exposed to oxalacetate or pyruvate. Other metabolites including glucose failed to stimulate anaerobic cation transport. Ouabaii abolished Na+-K+ movement in all 3 cases. Iodoacetate could not be simply inhibiting glycolysis because cation transport was abolished in oxygenated slices reconstituted with mitochondrial metabolites as well as in anaerobic slices. 2,4-Dinitrophenol inhibited transport identically in oxygen-, oxalacetate-, and pyruvate-treated slices at concentrations having no effect on transport or glycolysis in red cells. Although the relative importance of glycolytic or mitochondrial activity could not be assessed on the basis of these experiments, it is clearly evident that liver cells have the potential to generate sufficient ATP under anaerobiosis to drive cation transport.