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Mitochondrial Genome (mtDNA) Mutations that Generate Reactive Oxygen Species

Clem Jones Centre for Ageing Dementia Research, Queensland Brain Institute, The University of Queensland, 4072 Brisbane, Australia
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Antioxidants 2019, 8(9), 392; https://doi.org/10.3390/antiox8090392
Received: 19 August 2019 / Revised: 9 September 2019 / Accepted: 9 September 2019 / Published: 11 September 2019
(This article belongs to the Section ROS, RNS and RSS)
Mitochondria are critical for the energetic demands of virtually every cellular process within nucleated eukaryotic cells. They harbour multiple copies of their own genome (mtDNA), as well as the protein-synthesing systems required for the translation of vital subunits of the oxidative phosphorylation machinery used to generate adenosine triphosphate (ATP). Molecular lesions to the mtDNA cause severe metabolic diseases and have been proposed to contribute to the progressive nature of common age-related diseases such as cancer, cardiomyopathy, diabetes, and neurodegenerative disorders. As a consequence of playing a central role in cellular energy metabolism, mitochondria produce reactive oxygen species (ROS) as a by-product of respiration. Here we review the evidence that mutations in the mtDNA exacerbate ROS production, contributing to disease. View Full-Text
Keywords: mitochondrial DNA (mtDNA); oxidative stress; reactive oxygen species; mitochondrial disease; aging; cancer; neurodegeneration mitochondrial DNA (mtDNA); oxidative stress; reactive oxygen species; mitochondrial disease; aging; cancer; neurodegeneration
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MDPI and ACS Style

Hahn, A.; Zuryn, S. Mitochondrial Genome (mtDNA) Mutations that Generate Reactive Oxygen Species. Antioxidants 2019, 8, 392.

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