Enhanced expression and activity of xanthine oxidoreductase in the failing heart

J. W. De Jong, R. G. Schoemaker, R. De Jonge, P. Bernocchi, E. Keijzer, R. Harrison, H. S. Sharma, C. Ceconi

Research output: Contribution to journalArticlepeer-review


The molecular basis for heart failure is unknown, but oxidative stress is associated with the pathogenesis of the disease. We tested the hypothesis that the activity of xanthine oxidoreductase (XOR)*, a free-radical generating enzyme, increases in hypertrophied and failing heart. We studied XOR in two rat models: (1) The monocrotaline-induced right ventricular hypertrophy and failure model; (2) coronary artery ligation induced heart failure, with left ventricular failure and compensatory right ventricular hypertrophy at different stages at 3 and 8 weeks post-infarction, respectively. XOR activity was measured at 30°C and the reaction products were analysed by HPLC. In both models XOR activity in hypertrophic and control ventricles was similar. In the monocrotaline model, the hearts showed enhanced XOR activity in the failing right ventricle (65 ± 5 mU/g w/w), as compared to that in the unaffected left ventricle (47 ± 3 mU/g; P

Original languageEnglish
Pages (from-to)2083-2089
Number of pages7
JournalJournal of Molecular and Cellular Cardiology
Issue number11
Publication statusPublished - 2000


  • Free radicals
  • Heart failure
  • Hypertrophy
  • Infarction
  • Xanthine oxidase

ASJC Scopus subject areas

  • Molecular Biology
  • Cardiology and Cardiovascular Medicine


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