THE EFFECTS OF ANOXIA UPON ENERGY SOURCES AND SELECTED METABOLIC INTERMEDIATES IN THE BRAINS OF FISH, FROG AND TURTLE¹

TLDR

The study quantified ATP, phosphocreatine, glycogen, glucose, glycolytic intermediates, and lactate in fish, turtle, and frog brains and calculated the initial high‑energy phosphate consumption rate from their time‑dependent changes during decapitation‑induced anoxia. Compared with mammals, fish, turtle, and frog brains had 2–9× higher glycogen, a phosphocreatine:ATP ratio of 3, and similar other intermediates; during anoxia the high‑energy phosphate consumption rates were 1/20–1/50 of mouse brain, with first‑order depletion and progressive pH drop, phosphofructokinase and hexokinase inhibition.

Abstract

Abstract— The levels of the main cerebral energy reserves, ATP, P‐creatine, glycogen and glucose, and of several glycolytic intermediates and lactate, were measured in the brains of fish ( Carassius auratus ), turtle ( Pseudemys scripta elegans ) and frog ( Rana pipiens ). The levels of glycogen in these brains were 2‐9 times higher than those reported for mammals. In frog, cerebral glycogen levels were 35 per cent higher during the winter than in spring. The P‐creatine: ATP ratios were 3 instead of the more usual (mammalian) value of 1. The levels of other intermediates were similar to those found in mammalian brain. When anoxia was produced by decapitation, changes in the various substances measured were similar to those in mammalian brain, but were much slower. The initial rate at which high‐energy phosphate was used could be calculated from these changes. Values of 1.1 m‐equiv./kg/min for fish and frog and of 0.46 m‐equiv./kg/min for turtle were found, which are 1/20 and 1/50, respectively, of the rate in mouse brain. The rate of disappearance of high‐energy phosphate reserves followed first‐order kinetics for 4 hr in turtle and for at least an hour in the other species. Changes in metabolites as the experiment progressed were interpreted to indicate a progressively falling intracellular pH, prolonged inhibition of phosphofructokinase, and a long period of hexokinase inhibition.