Reye syndrome: serum-induced alterations in brain mitochondrial function are blocked by fatty-acid-free albumin.
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.
D000251:Adenosine Triphosphatases / Q000378:metabolism; D000818:Animals; D001769:Blood; D001921:Brain / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism*; D005230:Fatty Acids, Nonesterified / Q000494:pharmacology; D006801:Humans; D006863:Hydrogen-Ion Concentration; D008297:Male; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism*; D010085:Oxidative Phosphorylation / Q000187:drug effects; D010101:Oxygen Consumption / Q000187:drug effects; D051381:Rats; D012202:Reye Syndrome / Q000097:blood* / Q000503:physiopathology; D012709:Serum Albumin / Q000494:pharmacology*
D005230:Fatty Acids, Nonesterified; D012709:Serum Albumin; D000251:Adenosine Triphosphatases