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Oxidative Medicine and Cellular Longevity
Volume 2017, Article ID 3034245, 15 pages
Review Article

Cardiovascular Mitochondrial Dysfunction Induced by Cocaine: Biomarkers and Possible Beneficial Effects of Modulators of Oxidative Stress

1Department of Physiology and Pharmacology “Vittorio Erspamer”, Sapienza University of Rome, Rome, Italy
2Drug Addiction and Clinical Pharmacology Unit, University Hospital Umberto I, Sapienza University of Rome, Rome, Italy
3Department of Biochemical Sciences “Alessandro Rossi Fanelli”, Sapienza University of Rome, Rome, Italy
4Sussex Addiction Research and Intervention Centre (SARIC), School of Psychology, University of Sussex, Brighton BN1 9RH, UK

Correspondence should be addressed to Manuela Graziani; ti.1amorinu@inaizarg.aleunam

Received 1 December 2016; Revised 8 March 2017; Accepted 26 March 2017; Published 16 May 2017

Academic Editor: Daniela Giustarini

Copyright © 2017 Manuela Graziani et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Cocaine abuse has long been known to cause morbidity and mortality due to its cardiovascular toxic effects. The pathogenesis of the cardiovascular toxicity of cocaine use has been largely reviewed, and the most recent data indicate a fundamental role of oxidative stress in cocaine-induced cardiovascular toxicity, indicating that mitochondrial dysfunction is involved in the mechanisms of oxidative stress. The comprehension of the mechanisms involving mitochondrial dysfunction could help in selecting the most appropriate mitochondria injury biological marker, such as superoxide dismutase-2 activity and glutathionylated hemoglobin. The potential use of modulators of oxidative stress (mitoubiquinone, the short-chain quinone idebenone, and allopurinol) in the treatment of cocaine cardiotoxic effects is also suggested to promote further investigations on these potential mitochondria-targeted antioxidant strategies.