Effects of L and D-carnitine on brain energy metabolites in mice given sublethal doses of ammonium acetate.

Abstract

Previous studies in our laboratory have shown that L-carnitine suppresses seizures and alterations of brain energy metabolism in mice caused by hyperammonemia. The present study was done to exclude the effects of seizures on brain energy metabolism. When sublethal dose of ammonium acetate (12 mmol/kg b.wt.) was injected to mice, all mice survived without developing seizures, while clear increase of brain ammonia and alterations of brain energy metabolites were seen. In L-carnitine-treated animals, the levels of ammonia, AMP and lactate were lower and those of ATP and phosphocreatine were higher than in untreated animals. Treatment with D-carnitine also preserved the phosphocreatine level. This indicates that the improvement of brain energy metabolism by L-carnitine in hyperammonemia is not simply a result of the suppression of seizures, and that the "physiological" function of carnitine may not be the sole mechanism underlying this effect.

• Authors: M Matsuoka, H Igisu
• Journal: Pharmacology & toxicology (Pharmacol Toxicol) Vol. 72 Issue 3 Pg. 145-7 (Mar 1993) ISSN: 0901-9928 [Print] Denmark
• PMID: 8516263 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Acetates
• Lactates
• Phosphocreatine
• Lactic Acid
• Adenosine Monophosphate
• Ammonia
• Adenosine Triphosphate
• ammonium acetate
• Carnitine

Topics

• Acetates (toxicity)
• Adenosine Monophosphate (metabolism)
• Adenosine Triphosphate (metabolism)
• Ammonia (metabolism)
• Animals
• Brain (drug effects, metabolism)
• Carnitine (pharmacology, physiology)
• Energy Metabolism (drug effects)
• Injections, Intraperitoneal
• Lactates (metabolism)
• Lactic Acid
• Male
• Mice
• Phosphocreatine (metabolism)
• Stereoisomerism