Degradation of phospholipids by oxidative stress—Exceptional significance of cardiolipin

Abstract

The aim of this study was to investigate the effect of oxidative stress on mitochondrial phospholipids. In this context, this study investigated (i) the content of phosphatidylethanolamine (PE), phosphatidylcholine (PC) and cardiolipin (CL), (ii) the correlation of CL degradation with mitochondrial function and (iii) the correlation of CL degradation and CL oxidation. Oxidative stress induced by iron/ascorbate caused a dramatic decrease of these phospholipids, in which CL was the most sensitive phospholipid. Even moderate oxidative stress by hypoxia/reoxygenation caused a decrease in CL that was parallelled by a decrease in active respiration of isolated rat heart mitochondria. The relation between oxidative stress, CL degradation and CL oxidation was studied by in vitro treatment of commercially available CL with superoxide anion radicals and H2O2. The degradation of CL was mediated by H2O2 and required the presence of cytochrome c. Other peroxidases such as horse radish peroxidase and glutathione peroxidase had no effect. Cytochrome c in the presence of H2O2 caused CL oxidation. The data demonstrate that oxidative stress may cause degradation of phospholipids by oxidation, in particular CL; resulting in mitochondrial dysfunction.

Keywords::

• Phospholipids
• cardiolipin
• oxidative stress
• mitochondria
• cytochrome c

Acknowledgements

We are grateful to Mrs Heidemarie Faber for skillful technical assistance and to the expert statistician Professor Dr Siegfried Kropf (Institute of Biometry and Informatics, Medical Faculty, Otto-von-Guericke-University Magdeburg) for help and advice. This study was supported by COST Action B 35.

Declaration of interest: The authors report no conflict of interest. The authors alone are responsible for the content and writing of this paper.

This paper was first published online on Early Online on 26 October 2009.