Anoxic brain function: molecular mechanisms of metabolic depression.
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.
Brooks
S P
SP
Institute of Biochemistry, Carleton University Ottawa, Ontario, Canada.
Storey
K B
KB
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001921:Brain / Q000378:metabolism*; D002951:Citrates / Q000378:metabolism; D019343:Citric Acid; D005635:Fructosediphosphates / Q000378:metabolism; D000860:Hypoxia / Q000378:metabolism*; D007700:Kinetics; D010732:Phosphofructokinase-1 / Q000378:metabolism; D006005:Phosphorylases / Q000378:metabolism; D011770:Pyruvate Kinase / Q000378:metabolism; D014426:Turtles / Q000378:metabolism*
D002951:Citrates; D005635:Fructosediphosphates; D019343:Citric Acid; C027652:fructose 2,6-diphosphate; D000255:Adenosine Triphosphate; D006005:Phosphorylases; D010732:Phosphofructokinase-1; D011770:Pyruvate Kinase