An examination of the kinetic parameters of phosphofructokinase, pyruvate kinase and glycogen phosphorylase, and the cellular concentration of fructose 2,6-bisphosphate during anoxia in the turtle Pseudemys scripta showed that the total activity of glycogen phosphorylase, and the phosphofructokinase inhibition constants for citrate and ATP were decreased in anoxic turtle brain. These results suggest that the ability of turtle brain to survive extended periods of anoxia is the result of metabolic rate depression regulated, at the molecular level, by enzyme inactivation through anoxia-induced covalent modification.

Additional Metadata
Keywords (Pseudemys scripta), Brain metabolism, Covalent modification, Metabolic depression
Persistent URL dx.doi.org/10.1016/0014-5793(88)80419-8
Journal FEBS Letters
Citation
Brooks, S.P.J., & Storey, K. (1988). Anoxic brain function: Molecular mechanisms of metabolic depression. FEBS Letters, 232(1), 214–216. doi:10.1016/0014-5793(88)80419-8