Metabolic consequences of methylenecyclopropylglycine poisoning in rats


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MELDE, Klaus, Sandra JACKSON, Kim BARTLETT, H. Stanley A. SHERRATT, Sandro GHISLA, 1991. Metabolic consequences of methylenecyclopropylglycine poisoning in rats. In: Biochemical journal. 274(2), pp. 395-400. ISSN 0264-6021. eISSN 1470-8728. Available under: doi: 10.1042/bj2740395

@article{Melde1991Metab-6791, title={Metabolic consequences of methylenecyclopropylglycine poisoning in rats}, year={1991}, doi={10.1042/bj2740395}, number={2}, volume={274}, issn={0264-6021}, journal={Biochemical journal}, pages={395--400}, author={Melde, Klaus and Jackson, Sandra and Bartlett, Kim and Sherratt, H. Stanley A. and Ghisla, Sandro} }

1991 Melde, Klaus First publ. in: Biochemical journal 274 (1991), pp. 395-400 Jackson, Sandra eng Ghisla, Sandro Sherratt, H. Stanley A. 2011-03-24T17:29:12Z Jackson, Sandra Bartlett, Kim 2011-03-24T17:29:12Z Melde, Klaus Ghisla, Sandro Bartlett, Kim application/pdf Metabolic consequences of methylenecyclopropylglycine poisoning in rats terms-of-use Sherratt, H. Stanley A. We describe the effects of methylenecyclopropylglycine in fasted rats. A 75% decrease in the blood glucose concentration and an increase of lactate and pyruvate were observed 6 h after administration of 100 mg of this amino acid/kg. By contrast with the effects reported for hypoglycin [Williamson & Wilson (1965) Biochem. J. 94, 19c-21c], the plasma concentrations of ketone bodies decreased after administration of methylenecyclopropylglycine and the concentrations of branched-chain amino acids in the plasma were increased 6-fold. The oxidation of decanoylcarnitine or of palmitate was nearly completely inhibited in rat liver mitochondria from methylenecyclopropylglycine-poisoned rats. The activities of acetoacetyl-CoA and of 3-oxoacyl-CoA thiolase were decreased to 25% and < 10% of the controls. There was a pronounced aciduria, due to the excretion of dicarboxylic acids and of oxidation products of branched-chain amino acids. The accumulation of the toxic metabolite methylenecyclopropylformyl-CoA in the mitochondrial matrix was detected after administration of methylenecyclopropylglycine. Similarly we confirmed experimentally that methylenecyclopropylacetyl-CoA accumulates in mitochondria incubated with methylenecyclopropylpyruvate.

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