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M Costell

Publications and source records attributed to M Costell.

23 records · Page 2Linked to original sources
PubMed1984

Protective effect of L-carnitine on hyperammonemia.

Inborn errors of the urea cycle, liver malfunction and drug-induced hepatotoxicity are causes of life-threatening encephalopathies arising from hyperammonemia. L-Carnitine prevented entirely ammonia toxicity in mice when injected intraperitoneally 30 min before a lethal dose of ammonium acetate. Survival depends on the dose of L-carnitine injected, e.g., 0, 60, 70, 80 and 100% with 0, 1, 2, 8 and 16 mmol L-carnitine/kg, respectively. At the highest doses L-carnitine abolishes the convulsions that accompany acute ammonia intoxication. At lower doses it delayed their onset. The protective effect was associated with a marked decrease of blood ammonia, while in unprotected mice ammonemia was lethal in less than 15 min. When sustained hyperammonemia was induced by urease injections, protection was also obtained. The mechanism of protection is under investigation, however, since L-carnitine facilitates fatty acid entry into mitochondria, possibly ATP or reducing equivalents are increased.

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PubMed1984

Prevention of ammonia toxicity by L-carnitine: metabolic changes in brain.

L-Carnitine when injected in mice 30 min before an LD100 of ammonium acetate (12 mmol/kg body weight, intraperitoneal) reduced mortality (100% survival with 16 mmol L-carnitine/kg) and prevented the appearance of symptoms of ammonia toxicity. Brain ammonia decreased in the animals given L-carnitine. Ammonia decreased the levels of glutamate in brain; they were partially restored by L-carnitine, which also reduced the increase in brain glutamine in animals given only ammonia. The redox state of the brain was altered following ammonia intoxication. The ratio of lactate to pyruvate in the cytosol increased while that of glutamate to alpha-ketoglutarate in the mitochondria decreased. These ratios were partially restored by L-carnitine. The implications of these findings are discussed relative to the mechanism of ammonia toxicity.

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