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Sodium benzoate inhibits fatty acid oxidation in rat liver: effect on ammonia levels.

Abstract
Sodium benzoate inhibited PC and octanoic acid-mediated State 3 respiration rates by 39 and 29%, respectively, at 0.5 mM in isolated rat liver mitochondria. At 2 mM, benzoate did not affect State 3 respiration rates with either succinate or malate plus glutamate, indicating that it did not act as an uncoupler. The oxidation of palmitate and octanoate was inhibited by 39 and 54% at 2 mM benzoate in liver homogenates. Benzoate, at 10 mmol/kg caused significant decreases in the levels of hepatic ATP, CoA, and acetyl-CoA. Administration of sodium benzoate to rats caused a dose-dependent increase in hepatic ammonia levels. However, the inhibitory effect of benzoate on fatty acid oxidation is not mediated through ammonia since ammonium chloride, at 1 mM, did not inhibit PC or octanoate oxidation in mitochondria or their oxidation in liver homogenate. Our results warrant a reevaluation of the use of sodium benzoate in the treatment of hyperammonemia.
AuthorsS S Kalbag, A G Palekar
JournalBiochemical medicine and metabolic biology (Biochem Med Metab Biol) Vol. 40 Issue 2 Pg. 133-42 (Oct 1988) ISSN: 0885-4505 [Print] United States
PMID3190922 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Benzoates
  • Caprylates
  • Fatty Acids
  • Palmitates
  • Acetyl Coenzyme A
  • Ammonia
  • Adenosine Triphosphate
  • Benzoic Acid
  • Coenzyme A
Topics
  • Acetyl Coenzyme A (metabolism)
  • Adenosine Triphosphate (metabolism)
  • Ammonia (metabolism)
  • Animals
  • Benzoates (pharmacology)
  • Benzoic Acid
  • Caprylates (metabolism)
  • Coenzyme A (metabolism)
  • Fatty Acids (metabolism)
  • Liver (drug effects, metabolism)
  • Mitochondria, Liver (drug effects, metabolism)
  • Oxidation-Reduction
  • Oxygen Consumption (drug effects)
  • Palmitates (metabolism)
  • Rats
  • Rats, Inbred Strains

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