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Antioxidants 2016, 5(1), 7; doi:10.3390/antiox5010007

Mitochondrial Dysfunction in Cancer and Neurodegenerative Diseases: Spotlight on Fatty Acid Oxidation and Lipoperoxidation Products

1
Dipartimento di Scienze Cliniche e Biologiche, Università di Torino, Torino 10125, Italy
2
Dipartimento di Medicina e Scienze della Salute “V. Tiberio”, Università del Molise, Campobasso 86100, Italy
3
Dipartimento di Medicina Molecolare e Biotecnologie Mediche, Università di Napoli Federico II, Napoli 80131, Italy
4
Dipartimento di Scienze e Tecnologia del Farmaco, Università di Torino, Torino 10125, Italy
*
Author to whom correspondence should be addressed.
Academic Editors: Ethan J. Anderson and Jacques Robidoux
Received: 30 November 2015 / Revised: 22 January 2016 / Accepted: 5 February 2016 / Published: 19 February 2016
(This article belongs to the Special Issue Mitochondrial Fatty Acid Oxidation in Cell Signalling and Energetics)
View Full-Text   |   Download PDF [486 KB, uploaded 19 February 2016]   |  

Abstract

In several human diseases, such as cancer and neurodegenerative diseases, the levels of reactive oxygen species (ROS), produced mainly by mitochondrial oxidative phosphorylation, is increased. In cancer cells, the increase of ROS production has been associated with mtDNA mutations that, in turn, seem to be functional in the alterations of the bioenergetics and the biosynthetic state of cancer cells. Moreover, ROS overproduction can enhance the peroxidation of fatty acids in mitochondrial membranes. In particular, the peroxidation of mitochondrial phospholipid cardiolipin leads to the formation of reactive aldehydes, such as 4-hydroxynonenal (HNE) and malondialdehyde (MDA), which are able to react with proteins and DNA. Covalent modifications of mitochondrial proteins by the products of lipid peroxidation (LPO) in the course of oxidative cell stress are involved in the mitochondrial dysfunctions observed in cancer and neurodegenerative diseases. Such modifications appear to affect negatively mitochondrial integrity and function, in particular energy metabolism, adenosine triphosphate (ATP) production, antioxidant defenses and stress responses. In neurodegenerative diseases, indirect confirmation for the pathogenetic relevance of LPO-dependent modifications of mitochondrial proteins comes from the disease phenotypes associated with their genetic alterations. View Full-Text
Keywords: mitochondria; cancer; neurodegenerative diseases; fatty acid oxidation; lipoperoxidation products mitochondria; cancer; neurodegenerative diseases; fatty acid oxidation; lipoperoxidation products
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MDPI and ACS Style

Barrera, G.; Gentile, F.; Pizzimenti, S.; Canuto, R.A.; Daga, M.; Arcaro, A.; Cetrangolo, G.P.; Lepore, A.; Ferretti, C.; Dianzani, C.; Muzio, G. Mitochondrial Dysfunction in Cancer and Neurodegenerative Diseases: Spotlight on Fatty Acid Oxidation and Lipoperoxidation Products. Antioxidants 2016, 5, 7.

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