Abstract
Recently we showed that serum from Reye's Syndrome (RS) patients has an effect on the respiratory function and morphology of isolated rat liver mitochondria (mito.) suggesting the existence of a pathogenic serum factor. We now report further investigation into the biochemical mechanism of action of the serum factor. In vitro respiratory rates of isolated rat liver mito. were assessed polarographically as described previously (Science 197:908, 1977). State 4 respiration was markedly increased in the presence of RS serum as compared to control serum. To distinguish among several mechanisms for the increase in state 4 respiration, inhibitors of specific mito. functions were tested as possible antagonists of the RS effect. The inhibitors used were: eligomycin, an inhibitor of mito. ATPase, ruthenium red, which blocks mito. Ca++ transport; and three site-specific e− transport chain inhibitors: rotenone (site I), antimycin A (site II), KCN (site III). In each case RS serum was added to the assay in the presence of inhibitor to see if the usual stimulation of respiratory rate could be blocked. Of the inhibitors thus tested only KCN abolished the effect of RS serum. We concluded that the putative serum factor stimulated respiration by directly or indirectly reducing components of the e− transport chain at a point beyond phosphorylation site II. (Sup. by Chas. H. Hood Foundation)
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Aprille, J., Aslmakis, G. & Crawford, J. 392 THE EFFECT OF REYE'S SYNDROME SERUM ON MITOCHONDRIAL RESPIRATION IN VITRO. Pediatr Res 12 (Suppl 4), 429 (1978). https://doi.org/10.1203/00006450-197804001-00397
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DOI: https://doi.org/10.1203/00006450-197804001-00397