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Reye syndrome

Serum-induced alterations in brain mitochondrial function are blocked by fatty-acid-free albumin

Division of Neurology, Departments of Medicine and Physiological Chemistry, Ohio State University College of Medicine, Columbus.

Oxygen utilization and pH changes were monitored simultaneously in mitochondria isolated from rat brain. Addition of serum from four patients with Reye syndrome stimulated the resting respiratory rate, decreased respiratory control, stimulated ATPase activity, and decreased the rate of phosphorylation as measured by changes in pH. Serum from normal individuals did not have these effects. Convalescent serum from the three surviving patients showed a return of values toward normal. These changes were most marked with serum from the more deeply comatose patients. Contrary to a previous study of rat liver mitochondria, the changes were blocked by preincubation of the patients' sera with fatty-acid-free albumin. The serum factor responsible for the impairment in mitochondrial function may be a short- or medium-chain fatty acid.

Address correspondence and reprint requests to Dr. Ansevin, Division of Neurology, Departments of Medicine and Molecular Pathobiology, Northeastern Ohio Universities College of Medicine, 345 Oak Hill Avenue, Youngstown, OH 44501.

Accepted for publication June 29, 1979.

Presented at the thirty-first annual meeting of the American Academy of Neurology, Chicago, April 1979, and at the annual meeting of the National Reye's Syndrome Foundation, June 1979.

This investigation was supported by the National Institute of Neurological and Communicative Disorders and Stroke, National Institutes of Health, Grant No. 5 T 32 NS 07091–03.