Mitochondrial dysfunction increases oxidative stress and decreases chronological life span in fission yeast.

<h4>Background</h4>Oxidative stress is a probable cause of aging and associated diseases. Reactive oxygen species (ROS) originate mainly from endogenous sources, namely the mitochondria.<h4>Methodology/principal findings</h4>We analyzed the effect of aerobic metabolism on oxi...

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Autores principales:	Alice Zuin, Natalia Gabrielli, Isabel A Calvo, Sarela García-Santamarina, Kwang-Lae Hoe, Dong Uk Kim, Han-Oh Park, Jacqueline Hayles, José Ayté, Elena Hidalgo
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2008
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/070b013bcd0b41b28384e4e24064e0b9
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spelling	oai:doaj.org-article:070b013bcd0b41b28384e4e24064e0b92021-11-25T06:11:22ZMitochondrial dysfunction increases oxidative stress and decreases chronological life span in fission yeast.1932-620310.1371/journal.pone.0002842https://doaj.org/article/070b013bcd0b41b28384e4e24064e0b92008-07-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/18665268/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Background</h4>Oxidative stress is a probable cause of aging and associated diseases. Reactive oxygen species (ROS) originate mainly from endogenous sources, namely the mitochondria.<h4>Methodology/principal findings</h4>We analyzed the effect of aerobic metabolism on oxidative damage in Schizosaccharomyces pombe by global mapping of those genes that are required for growth on both respiratory-proficient media and hydrogen-peroxide-containing fermentable media. Out of a collection of approximately 2700 haploid yeast deletion mutants, 51 were sensitive to both conditions and 19 of these were related to mitochondrial function. Twelve deletion mutants lacked components of the electron transport chain. The growth defects of these mutants can be alleviated by the addition of antioxidants, which points to intrinsic oxidative stress as the origin of the phenotypes observed. These respiration-deficient mutants display elevated steady-state levels of ROS, probably due to enhanced electron leakage from their defective transport chains, which compromises the viability of chronologically-aged cells.<h4>Conclusion/significance</h4>Individual mitochondrial dysfunctions have often been described as the cause of diseases or aging, and our global characterization emphasizes the primacy of oxidative stress in the etiology of such processes.Alice ZuinNatalia GabrielliIsabel A CalvoSarela García-SantamarinaKwang-Lae HoeDong Uk KimHan-Oh ParkJacqueline HaylesJosé AytéElena HidalgoPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 3, Iss 7, p e2842 (2008)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Alice Zuin Natalia Gabrielli Isabel A Calvo Sarela García-Santamarina Kwang-Lae Hoe Dong Uk Kim Han-Oh Park Jacqueline Hayles José Ayté Elena Hidalgo Mitochondrial dysfunction increases oxidative stress and decreases chronological life span in fission yeast.
description	<h4>Background</h4>Oxidative stress is a probable cause of aging and associated diseases. Reactive oxygen species (ROS) originate mainly from endogenous sources, namely the mitochondria.<h4>Methodology/principal findings</h4>We analyzed the effect of aerobic metabolism on oxidative damage in Schizosaccharomyces pombe by global mapping of those genes that are required for growth on both respiratory-proficient media and hydrogen-peroxide-containing fermentable media. Out of a collection of approximately 2700 haploid yeast deletion mutants, 51 were sensitive to both conditions and 19 of these were related to mitochondrial function. Twelve deletion mutants lacked components of the electron transport chain. The growth defects of these mutants can be alleviated by the addition of antioxidants, which points to intrinsic oxidative stress as the origin of the phenotypes observed. These respiration-deficient mutants display elevated steady-state levels of ROS, probably due to enhanced electron leakage from their defective transport chains, which compromises the viability of chronologically-aged cells.<h4>Conclusion/significance</h4>Individual mitochondrial dysfunctions have often been described as the cause of diseases or aging, and our global characterization emphasizes the primacy of oxidative stress in the etiology of such processes.
format	article
author	Alice Zuin Natalia Gabrielli Isabel A Calvo Sarela García-Santamarina Kwang-Lae Hoe Dong Uk Kim Han-Oh Park Jacqueline Hayles José Ayté Elena Hidalgo
author_facet	Alice Zuin Natalia Gabrielli Isabel A Calvo Sarela García-Santamarina Kwang-Lae Hoe Dong Uk Kim Han-Oh Park Jacqueline Hayles José Ayté Elena Hidalgo
author_sort	Alice Zuin
title	Mitochondrial dysfunction increases oxidative stress and decreases chronological life span in fission yeast.
title_short	Mitochondrial dysfunction increases oxidative stress and decreases chronological life span in fission yeast.
title_full	Mitochondrial dysfunction increases oxidative stress and decreases chronological life span in fission yeast.
title_fullStr	Mitochondrial dysfunction increases oxidative stress and decreases chronological life span in fission yeast.
title_full_unstemmed	Mitochondrial dysfunction increases oxidative stress and decreases chronological life span in fission yeast.
title_sort	mitochondrial dysfunction increases oxidative stress and decreases chronological life span in fission yeast.
publisher	Public Library of Science (PLoS)
publishDate	2008
url	https://doaj.org/article/070b013bcd0b41b28384e4e24064e0b9
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Mitochondrial dysfunction increases oxidative stress and decreases chronological life span in fission yeast.

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