FLUOROACETATE AND THE METABOLISM OF AMMONIA IN BRAIN

Publisher Website
Google Scholar
Abstract
Sodium fluoroacetate, at concentrations of 1 m[image] or less, which have no effect on the respiration of rat-brain-cortex slices incubated in Krebs-Ringer phosphate medium containing glucose, suppresses the formation of C14-labelled glutamine from [C146]glucose, the effect being greater in a medium containing 105 m-equiv. of K+ ions/l than in one containing 5 m-equiv. of K+ ions/l. There is a concomitant increase in the amount of C14-labelled glutamate formed. Sodium fluoroacetate (1 m[image]) suppresses the accelerating action of NH4+ ions on the rates of oxygen consumption and of the formation of C14-labelled glutamine (from[C14g]glucose) by the brain-cortex slices. Sodium fluoroacetate (1 m[image]) increases the amount of free ammonia in the brain-cortex slices after incubation in the presence of glucose for 1 hr. at 37[degree]. The yields of C14-labelled glutamine and C14-labelled aspartate derived from [C14 5]glutamate by rat-brain-cortex slices, incubated in Krebs-Ringer phosphate medium containing glucose, are diminished in the presence of sodium fluoroacetate (1 m[image]). The addition of Amytal (0-5 m[image]) diminishes the enhanced rate of formation of C14-labelled glutamate from [C14 6]glucose due to 1 m[image]-sodium fluoroacetate. The results are consistent with the conclusion that sodium fluoroacetate, at concentrations of 1 m[image] or less, inhibits the utilization of NH4+ ions by rat-brain-cortex slices respiring in Krebs-Ringer phosphate medium containing glucose.