The impact of oxidative stress on Arabidopsis mitochondria

Treatment of <em>Arabidopsis</em> cell culture for 16 h with H₂O₂ menadione or antimycin A induced an oxidative stress decreasing growth rate and increasing DCF fluorescence and lipid peroxidation products. Treated cells remained viable and maintained significant respiratory rates. Mitoc...

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Main Authors: Sweetlove, L, Heazlewood, J, Herald, V, Holtzapffel, R, Day, D, Leaver, C, Millar, A
Other Authors: Society for Experimental Biology
Format: Journal article
Language:English
Published: Blackwell Publishing Ltd 2002
Subjects:
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author Sweetlove, L
Heazlewood, J
Herald, V
Holtzapffel, R
Day, D
Leaver, C
Millar, A
author2 Society for Experimental Biology
author_facet Society for Experimental Biology
Sweetlove, L
Heazlewood, J
Herald, V
Holtzapffel, R
Day, D
Leaver, C
Millar, A
author_sort Sweetlove, L
collection OXFORD
description Treatment of <em>Arabidopsis</em> cell culture for 16 h with H₂O₂ menadione or antimycin A induced an oxidative stress decreasing growth rate and increasing DCF fluorescence and lipid peroxidation products. Treated cells remained viable and maintained significant respiratory rates. Mitochondrial integrity was maintained, but accumulation of alternative oxidase and decreased abundance of lipoic acid-containing components during several of the treatmnets indicated oxidative stress. Analysis of the treatments was undertaken by IEF/SDS-PAGE, comparison of protein spot abundances and tandem mass spectrometry. A set of 25 protein spots increased &gt; 3-fold in H₂O₂/ manadione treatments, a subset of these increased in antimycin A-treated samples. A set of 10 protein spots decreased significantly during stress treatments. A specific set of mitochondrial proteins were degraded by stress treatments. These damaged components included subunits of ATP synthase, complex I, succinyl CoA ligase, aconitase, and pyruvate and 2-oxoglutarate dehydrogenase complexes. Nine increased proteins represented products of different genes not found in control mitochondria. One is directly involved in antioxidant defense, a mitochondrial thioredoxin-dependent peroxidase, while another, a thioredoxin reductase-dependent protein disulphide isomerase, is required for protein disulfide redox homeostasis. Several others are generally considered to be extramitochondrial but are clearly present in a highly purified mitochondrial fraction used in this study and are known to play roles in stress response. Using H₂O₂ as a model stress, further work revealed that this treatment induced a protease activity in isolated mitochondria, putatively responsible for the degradation of oxidatively damaged mitochondrial proteins and that O₂ consumption by mitochondria was significantly decreased by H₂O₂ treatment.
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spelling oxford-uuid:27b7559c-6050-4c04-9537-44845d5abcc92022-03-26T12:08:32ZThe impact of oxidative stress on Arabidopsis mitochondriaJournal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:27b7559c-6050-4c04-9537-44845d5abcc9Plant SciencesEnglishOxford University Research Archive - ValetBlackwell Publishing Ltd2002Sweetlove, LHeazlewood, JHerald, VHoltzapffel, RDay, DLeaver, CMillar, ASociety for Experimental BiologyTreatment of <em>Arabidopsis</em> cell culture for 16 h with H₂O₂ menadione or antimycin A induced an oxidative stress decreasing growth rate and increasing DCF fluorescence and lipid peroxidation products. Treated cells remained viable and maintained significant respiratory rates. Mitochondrial integrity was maintained, but accumulation of alternative oxidase and decreased abundance of lipoic acid-containing components during several of the treatmnets indicated oxidative stress. Analysis of the treatments was undertaken by IEF/SDS-PAGE, comparison of protein spot abundances and tandem mass spectrometry. A set of 25 protein spots increased &gt; 3-fold in H₂O₂/ manadione treatments, a subset of these increased in antimycin A-treated samples. A set of 10 protein spots decreased significantly during stress treatments. A specific set of mitochondrial proteins were degraded by stress treatments. These damaged components included subunits of ATP synthase, complex I, succinyl CoA ligase, aconitase, and pyruvate and 2-oxoglutarate dehydrogenase complexes. Nine increased proteins represented products of different genes not found in control mitochondria. One is directly involved in antioxidant defense, a mitochondrial thioredoxin-dependent peroxidase, while another, a thioredoxin reductase-dependent protein disulphide isomerase, is required for protein disulfide redox homeostasis. Several others are generally considered to be extramitochondrial but are clearly present in a highly purified mitochondrial fraction used in this study and are known to play roles in stress response. Using H₂O₂ as a model stress, further work revealed that this treatment induced a protease activity in isolated mitochondria, putatively responsible for the degradation of oxidatively damaged mitochondrial proteins and that O₂ consumption by mitochondria was significantly decreased by H₂O₂ treatment.
spellingShingle Plant Sciences
Sweetlove, L
Heazlewood, J
Herald, V
Holtzapffel, R
Day, D
Leaver, C
Millar, A
The impact of oxidative stress on Arabidopsis mitochondria
title The impact of oxidative stress on Arabidopsis mitochondria
title_full The impact of oxidative stress on Arabidopsis mitochondria
title_fullStr The impact of oxidative stress on Arabidopsis mitochondria
title_full_unstemmed The impact of oxidative stress on Arabidopsis mitochondria
title_short The impact of oxidative stress on Arabidopsis mitochondria
title_sort impact of oxidative stress on arabidopsis mitochondria
topic Plant Sciences
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