Depression of oxidative metabolism of aspirin in mice via an interferon-associated mechanism in relation to Reye's syndrome.
Interferon synthesis was induced in inbred strains of mice with either polyriboinosinic-polyribocytidylic acid or Newcastle disease virus. The strains, BALB/cBy and C57BL/6By, respond to Newcastle disease virus by producing 'low' and 'high' levels of serum interferon, respectively. 24 h after interferon induction mice received [carboxyl-14C]-aspirin orally. The metabolic conjugation of aspirin was little changed after either treatment while the urinary excretion of gentisic acid, a minor product of metabolic oxidation, was significantly depressed after polyriboinosinic-polyribocytidylic acid in both strains and in C57BL/6By mice after Newcastle disease virus. The results suggest that such a metabolic impairment in aspirin metabolism would not significantly affect salicylate clearance and hence are unlikely to be directly related to the aetiology of Reye's syndrome which has been associated with both a prodromal viral infection and aspirin therapy.
D000818:Animals; D001241:Aspirin / Q000378:metabolism*; D007372:Interferons / Q000378:metabolism*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D009522:Newcastle disease virus; D010084:Oxidation-Reduction; D011070:Poly I-C / Q000494:pharmacology; D012202:Reye Syndrome / Q000378:metabolism*
D007372:Interferons; D011070:Poly I-C; D001241:Aspirin