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Oxidative Medicine and Cellular Longevity
Volume 2013 (2013), Article ID 971024, 10 pages
http://dx.doi.org/10.1155/2013/971024
Review Article

Mitochondrial Dysfunctions and Altered Metals Homeostasis: New Weapons to Counteract HCV-Related Oxidative Stress

1Department of Internal Medicine and Medical Specialties, “Sapienza” University of Rome, Via del Policlinico 155, 00161 Rome, Italy
2Francesco Balsano Foundation, Via G.B. Martini 6, 00198 Rome, Italy
3Institute of Molecular Biology and Pathology (IBPM); CNR, Piazzale Aldo Moro 7, 00185 Rome, Italy

Received 10 June 2013; Revised 18 October 2013; Accepted 28 October 2013

Academic Editor: Peter Shaw

Copyright © 2013 Mario Arciello 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.

Abstract

The hepatitis C virus (HCV) infection produces several pathological effects in host organism through a wide number of molecular/metabolic pathways. Today it is worldwide accepted that oxidative stress actively participates in HCV pathology, even if the antioxidant therapies adopted until now were scarcely effective. HCV causes oxidative stress by a variety of processes, such as activation of prooxidant enzymes, weakening of antioxidant defenses, organelle damage, and metals unbalance. A focal point, in HCV-related oxidative stress onset, is the mitochondrial failure. These organelles, known to be the “power plants” of cells, have a central role in energy production, metabolism, and metals homeostasis, mainly copper and iron. Furthermore, mitochondria are direct viral targets, because many HCV proteins associate with them. They are the main intracellular free radicals producers and targets. Mitochondrial dysfunctions play a key role in the metal imbalance. This event, today overlooked, is involved in oxidative stress exacerbation and may play a role in HCV life cycle. In this review, we summarize the role of mitochondria and metals in HCV-related oxidative stress, highlighting the need to consider their deregulation in the HCV-related liver damage and in the antiviral management of patients.