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.
|Journal||Journal of Cardiovascular Pharmacology|
|Issue number||SUPPL. 1|
|Publication status||Published - 1997|
- Heart mitochondria
- Lipid peroxidation
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine