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Oxidative Medicine and Cellular Longevity
Volume 2014, Article ID 541230, 27 pages
http://dx.doi.org/10.1155/2014/541230
Review Article

Oxidative Stress and Mitochondrial Dysfunction across Broad-Ranging Pathologies: Toward Mitochondria-Targeted Clinical Strategies

1Cancer Research Centre at Mercogliano (CROM), Istituto Nazionale Tumori Fondazione G. Pascale-IRCCS, 80131 Naples, Italy
2Research Laboratory, Dental School, Sevilla University, 41009 Sevilla, Spain
3Department of Chemical Sciences, Federico II University, 80126 Naples, Italy
4National Research Council, Institute of Biomembranes and Bioenergetics, 70126 Bari, Italy
5CIBERER, University of Valencia-INCLIVA, 46010 Valencia, Spain
6“Vinca” Institute of Nuclear Sciences, University of Belgrade, 11070 Belgrade, Serbia
7Department of Clinical and Dental Sciences, Polytechnical University of Marche, 60100 Ancona, Italy
8Department of Genetics, ASL Napoli 1, 80136 Naples, Italy

Received 13 December 2013; Accepted 24 February 2014; Published 4 May 2014

Academic Editor: Cinzia Signorini

Copyright © 2014 Giovanni Pagano 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

Beyond the disorders recognized as mitochondrial diseases, abnormalities in function and/or ultrastructure of mitochondria have been reported in several unrelated pathologies. These encompass ageing, malformations, and a number of genetic or acquired diseases, as diabetes and cardiologic, haematologic, organ-specific (e.g., eye or liver), neurologic and psychiatric, autoimmune, and dermatologic disorders. The mechanistic grounds for mitochondrial dysfunction (MDF) along with the occurrence of oxidative stress (OS) have been investigated within the pathogenesis of individual disorders or in groups of interrelated disorders. We attempt to review broad-ranging pathologies that involve mitochondrial-specific deficiencies or rely on cytosol-derived prooxidant states or on autoimmune-induced mitochondrial damage. The established knowledge in these subjects warrants studies aimed at elucidating several open questions that are highlighted in the present review. The relevance of OS and MDF in different pathologies may establish the grounds for chemoprevention trials aimed at compensating OS/MDF by means of antioxidants and mitochondrial nutrients.