REYES-SYNDROME SIMULACRA IN LIVER OF MICE AFTER TREATMENT WITH CHEMICAL-AGENTS AND ENCEPHALOMYOCARDITIS VIRUS

  • 1 January 1981
    • journal article
    • research article
    • Vol. 45  (1) , 89-109
Abstract
In children with Reye''s syndrome, liver specimens exhibit the following characteristics: mitochondrial disfiguration, fatty infiltration, decreased activity of carbamyl phosphate synthetase and of ornithine transcarbamylase, histochemically reduced activity of succinic dehydrogenase and cytochrome oxidase and depletion of glycogen. An animal model for Reye''s syndrome was created by treating mice with encephalomyocarditis virus and/or salicylate, fructose, Atlox (A), butylated hydroxytoluene (B), pentachlorophenol and an equal mixture of B and monosodium stearate. Liver specimens were then examined for the listed characteristics and for the activity of argininosuccinic lyase, arginase, phosphorylase and glucose-6-phosphatase. Results were obtained in livers of mice treated with virus and A or virus and B. A significant (P < 0.05) reduction was found [except for ornithine transcarbamylase (A)] to the following levels (in percentage of normal mean): carbamyl phosphate synthetase (A, 79%; B, 57%); ornithine transcarbamylase (A, 91%; B, 75%); glycogen (A, 26%; B, 37%). Simultaneous morphologic analysis of these liver specimens indicated mitochondrial disfiguration, absence of dense granules, fatty infiltration and normal activity of succinic dehydrogenase and cytochrome oxidase. The induction of Reye''s syndrome-like features in mouse liver may be useful for the study of disease mechanisms and therapy.

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