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Reye's Syndrome (RS) serum added to isolated rat liver mitochondria caused a stimulation of O2 consumption [BBRC 79:1122 (1977)]. This suggested a metabolic toxin in the serum with activity
against mitochondria. Recently, the substance responsible for the serum activity was identified as uric acid [BBRC 94:381 (1980)]. However, it appeared that uric acid had no direct effect on
mitochondria. Instead, it was suspected that the stimulation of O2 consumption was a result of the oxidation of the added uric acid by peroxisomes, which are usually present with rat liver
mitochondria prepared by differential centrifugation. This was confirmed by separating mitochondria and peroxisomes, in which case the serum effect followed the peroxisomal fraction. Further
study showed that all of the serum activity detected in the bioassay was attributable to uric acid oxidation. The concentration of uric acid in serum was directly correlated with the
magnitude of the serum effect on O2 utilization, and uricase treatment of serum abolished its effect on O2 consumption. In summary, the particular bioassay used in these studies detected
uric acid, which is not a genuine pathogenic factor in RS. The search for “serum factors” should be continued using this general approach, but employing different bioassays to detect adverse
effects on metabolic function. (Supp. by NIH NS 14936)
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