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- W1996582703 abstract "In order to search into the underlying mechanisms of ECG changes suggestive of ischemia observed in humans and in rabbits after administration of 5-fluorouracil (5-FU), experiments were performed in anesthetized open-chest guinea pigs. The substance produced similar ECG changes in this species as well, after a rather long latent period of around 3 hours after intravenous administration. The incidence of ECG abnormality in animals given 60 mg/kg was 7/7, while that in animals given 30 mg/kg was 4/9. With 10–20 mg/kg, ECG changes were not observed during an experimental period as long as 5 hours. Associated with these ECG changes, a depletion of the high-energy phosphate compounds of the ventricular myocardium was observed. Analysis of tricarboxylic acid cycle (TCA cycle) intermediates revealed an accumulation of citrate within the myocardium, suggesting a malfunction of TCA cycle resulting from an inhibition of aconitase by fluorocitrate, as a cause of depletion of the high-energy phosphates. It is highly probable that the accumulation of citrate was due to the formation of fluoroacetate, an inhibitor of aconitase, from 5-FU via α-fluoro-β-alanine, a major degradation product of 5-FU, for it is known that β-alanine is usually converted to acetate." @default.
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- W1996582703 date "1980-01-01" @default.
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- W1996582703 title "Cardiotoxic effects of 5-fluorouracil in the guinea pig." @default.
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- W1996582703 doi "https://doi.org/10.1254/jjp.30.871" @default.
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