HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Petrosillo, G. Articles by Ruggiero, F. M. Search for Related Content PubMed PubMed Citation Articles by Petrosillo, G. Articles by Ruggiero, F. M.

Protective effect of melatonin against mitochondrial dysfunction associated with cardiac ischemia- reperfusion: role of cardiolipin

G. Petrosillo^*, N. Di Venosa, M. Pistolese^*, G. Casanova^*, E. Tiravanti, G. Colantuono, A. Federici, G. Paradies^*,1 and F. M. Ruggiero^*

^* Department of Biochemistry and Molecular Biology and CNR Institute of Biomembranes and Bioenergetics,
Department of Emergency and Transplantation, and
Department of Pharmacology and Human Physiology University of Bari, Bari Italy

¹ Correspondence: E-mail: g.paradies{at}biologia.uniba.it

Reactive oxygen species (ROS) are considered an important factor in ischemia/reperfusion injury to cardiac myocytes. Mitochondrial respiration, mainly at the level of complex I and III, is an important source of ROS generation and hence a potential contributor of cardiac reperfusion injury. Appropriate antioxidant strategies could be particularly useful to limit this ROS generation and associated mitochondrial dysfunction. Melatonin has been shown to effectively protect against ischemic-reperfusion myocardial damage. The mechanism by which melatonin exerts this cardioprotective effect is not well established. In the present study we examined the effects of melatonin on various parameters of mitochondrial bioenergetics in a Langerdoff isolated perfused rat heart model. After isolation of mitochondria from control, ischemic-reperfused and melatonin-treated ischemic-reperfused rat heart, various bioenergetic parameters were evaluated such as rates of mitochondrial oxygen consumption, complex I and complex III activity, H₂O₂ production as well as the degree of lipid peroxidation, cardiolipin content, and cardiolipin oxidation. We found that reperfusion significantly altered all these mitochondrial parameters, while melatonin treatment had strong protective effect attenuating these alterations. This effect appears to be due, at least in part, to the preservation, by ROS attack, of the content and integrity of cardiolipin molecules which play a pivotal role in mitochondrial bioenergetics. Protection of mitochondrial dysfunction was associated with an improvement of post-ischemic hemodynamic function of the heart. Melatonin had also strong protective effect against oxidative alterations to complex I and III as well as to cardiolipin in isolated mitochondria.—Petrosillo, G., Di Venosa, N., Pistolese, M., Casanova, G., Tiravanti, E., Colantuono, G., Federici, A., Paradies, G., Ruggiero, F. M. Protective effect of melatonin against mitochondrial dysfunction associated with cardiac ischemia-reperfusion: role of cardiolipin.

Key Words: ROS • mitochondria • MPT

This article has been cited by other articles:

				T. Walther, C. Tschope, A. Sterner-Kock, D. Westermann, S. Heringer-Walther, A. Riad, A. Nikolic, Y. Wang, L. Ebermann, W.-E. Siems, et al. Accelerated Mitochondrial Adenosine Diphosphate/Adenosine Triphosphate Transport Improves Hypertension-Induced Heart Disease Circulation, January 23, 2007; 115(3): 333 - 344. [Abstract] [Full Text] [PDF]

				A. J. Chicco and G. C. Sparagna Role of cardiolipin alterations in mitochondrial dysfunction and disease Am J Physiol Cell Physiol, January 1, 2007; 292(1): C33 - C44. [Abstract] [Full Text] [PDF]