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.
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Authors | S S Kalbag, A G Palekar |
Journal | Biochemical medicine and metabolic biology
(Biochem Med Metab Biol)
Vol. 40
Issue 2
Pg. 133-42
(Oct 1988)
ISSN: 0885-4505 [Print] United States |
PMID | 3190922
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Benzoates
- Caprylates
- Fatty Acids
- Palmitates
- Acetyl Coenzyme A
- Ammonia
- Adenosine Triphosphate
- Benzoic Acid
- Coenzyme A
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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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