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September 1973

Aberrant Behavior of Phosphofructokinase From Otosclerotic Stapedes: Biochemical Evidence and the Metabolic Consequences

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).

Arch Otolaryngol. 1973;98(3):191-195. doi:10.1001/archotol.1973.00780020199012

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.

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