Effect of Salicylate on Ureagenesis in Rat Liver

Am, Glasgow; Hp, Chase

doi:10.3181/00379727-155-39742

Cited by 6 publications

(4 citation statements)

References 3 publications

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“…Aspirin treatment prior to presentation of the arginine-deficient diet (Table 1) (28,29) and inhibits ATP/ADP exchange (29) in isolated liver mitochondria. It hinders the urea cycle by inhibiting citrulline synthesis in rat liver slices (30). Ammonia freely enters isolated mitochondria, causing swelling (31), and can react withx-ketoglutarate and NADH to form glutamate.…”

mentioning

confidence: 99%

Interactions of aspirin and other potential etiologic factors in an animal model of Reye syndrome.

Deshmukh¹,

Maassab²,

Mason³

1982

Proc. Natl. Acad. Sci. U.S.A.

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Recent studies of Reye syndrome (RS) patients have suggested aspirin treatment as a possible factor in the etiology of this often fatal childhood disorder. The relationship of aspirin treatment to other factors that have been strongly implicated (influenza, ammonia toxicity) cannot be examined directly in patients because aspirin treatment is usually initiated by family members in the prodromal period before RS is diagnosed. In this report we describe the use ofan animal model for RS in examining the interactions of these several potential etiological factors. Hyperammonemia and coma were produced in young male ferrets by a brief feeding of an arginine-deficient diet. The effects of influenza infection or aspirin treatment (or both) of control and hyperammonemic ferrets on their serum levels of ammonia, glutamic-oxaloacetic transaminase (GOT; L-aspartate: 2-oxoglutarate aminotransferase, EC 2.6.1.1), ornithine carbamoyltransferase (OCT; carbamoylphosphate: L-ornithine carbamoyltransferase, EC 2.1.3.3), bilirubin, and salicylate were studied. Liver levels of lipids, proteins, and several urea-cycle enzymes were also determined in the comatose ferrets and compared with those of untreated controls and of controls treated with influenza or aspirin, or both. Synergism of these three factors (hyperammonemia, influenza infection, and aspirin treatment) in causing RS-like alterations in these parameters was observed.

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confidence: 99%

Interactions of aspirin and other potential etiologic factors in an animal model of Reye syndrome.

Deshmukh¹,

Maassab²,

Mason³

1982

Proc. Natl. Acad. Sci. U.S.A.

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“…Both changes are reversible and only evident at large doses of salicylate.Elevatedlevelsof serum transaminases, hepatic steatosis, impaired urea genesis and disturbed lipid metabolism also found in animals fed high aspirin doses [333][334][335]. Both changes are reversible and only evident at large doses of salicylate.Elevatedlevelsof serum transaminases, hepatic steatosis, impaired urea genesis and disturbed lipid metabolism also found in animals fed high aspirin doses [333][334][335].…”

Section: Mechanisms Of Aspirin Actionmentioning

confidence: 94%

Toxicity and Drug Safety

Schrör

2008

Acetylsalicylic Acid

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“…Salicylates inhibit hepatic aminotransferases, which increases blood amino acid levels and can produce aminoaciduria 6 . Salicylates also impair the urea cycle both indirectly, by inhibiting the respiratory chain, and directly, by suppressing production of ornithine transcarbamylase; these effects explain both patients’ hyperammonaemia 7 …”

mentioning

confidence: 99%

“…The mother of Patient 1 admitted using two to three 15 g tubes per week over a long period. This equates to twice the minimum daily dose reported to have caused toxicity following chronic ingestion 7 …”

mentioning

confidence: 99%