Effects of lercanidipine on Fe2+-induced mitochondrial lipid peroxidation

Palmira Bernocchi, Claudio Ceconi, Anna Cargnoni, Paolo Pedersini, Antonella Boraso, Salvatore Curello, Roberto Ferrari

Research output: Contribution to journalArticlepeer-review


Cardiac mitochondria were incubated with ferrous ion as catalyst of lipid peroxidation. Ferrous ions induced an increase in malondialdehyde (MDA) formation (from 1.24 ± 0.51 to 7.84 ± 1.66 nmol/mg protein; p <0.01), and a significant reduction (p <0.001) in mitochondrial oxygen consumption and calcium transporting capacity. Lercanidipine was used at two concentrations; 10-7 and 10-8 M. Administration of lercanidipine at 10-8 M failed significantly prevent lipid peroxidation and mitochondrial damage, despite a trend toward protection. At the higher concentration of 10-7 M, lercanidipine exerted significant protection because it reduced the formation of MDA (from 7.84 ± 1.66 to 4.19 ± 1.15 nmol/mg protein; p <0.01), significantly improved all indices of mitochondrial function (RCl, QO2/3, QO2/4, and ADP/O), and prevented the iron-mediated changes in mitochondrial calcium accumulation and retention capacity. These data indicate that lercanidipine at submicromolar concentrations prevents heart mitochondrial damage induced by lipid peroxidation.

Original languageEnglish
JournalJournal of Cardiovascular Pharmacology
Issue numberSUPPL. 1
Publication statusPublished - 1997


  • Heart mitochondria
  • Lercanidipine
  • Lipid peroxidation
  • Malondialdehyde

ASJC Scopus subject areas

  • Pharmacology
  • Cardiology and Cardiovascular Medicine


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