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Aberrant Behavior of Phosphofructokinase From Otosclerotic StapedesBiochemical Evidence and the Metabolic Consequences
Charles E. Holdsworth, PhD;
Gerald L. Endahl, PhD;
Nathaniel Soifer, MD;
Keith E. Richardson, PhD
Arch Otolaryngol. 1973;98(3):191-195.
Abstract
The sensitivity of phosphofructokinase to stimulation by sulfate, adenosine monophosphate, and cyclic adenosine monophosphate is decreased in otosclerosis. The enzyme is unresponsive to inhibition by a citrate and markedly stimulated by lactate, normally not an effector.
The evidence suggests that aberrant phosphofructokinase is operative in otosclerosis. This would cause defective regulation of glycolysis and a consequent imbalance between the anaerobic and aerobic phases of metabolism. Evidence from this and other studies supports the conclusion that otosclerotic bone is abnormally geared to a primarily aerobic metabolism.
Author Affiliations
Columbus, Ohio; Los Angeles; Dayton, Ohio; Columbus, Ohio
From the Department of Physiological Chemistry, Ohio State University, Columbus, Ohio (Drs. Holdsworth and Richardson); University of Southern California, Los Angeles (Dr. Endahl); and the Good Samaritan Hospital, Dayton, Ohio (Dr. Soifer).
Footnotes
Accepted for publication Aug 24, 1972.
Reprint requests to 6400 Brushwood Ct, Dayton, OH 45415 (Dr. Holdsworth).
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