Mitochondrial H2O2 release does not directly cause damage to chromosomal DNA

Reactive Oxygen Species (ROS) derived from mitochondrial respiration are frequently cited as a major source of chromosomal DNA mutations that contribute to cancer development and aging. However, experimental evidence showing that ROS released by mitochondria can directly damage nuclear DNA is largel...

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Published inNature communications Vol. 15; no. 1; p. 2725
Main Authors van Soest, Daan M. K., Polderman, Paulien E., den Toom, Wytze T. F., Keijer, Janneke P., van Roosmalen, Markus J., Leyten, Tim M. F., Lehmann, Johannes, Zwakenberg, Susan, De Henau, Sasha, van Boxtel, Ruben, Burgering, Boudewijn M. T., Dansen, Tobias B.
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 28.03.2024
Nature Publishing Group
Nature Portfolio
Subjects
13/31
13/95
14/19
45/23
631/337/1427/2566
631/80/86/2366
82/1
96/35
96/63
Aging
Cancer
Cell cycle
Damage localization
Deoxyribonucleic acid
DNA
DNA damage
Humanities and Social Sciences
Hydrogen peroxide
Mitochondria
Mitochondrial DNA
multidisciplinary
Mutation
Nucleosomes
Reactive oxygen species
Science
Science (multidisciplinary)
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Abstract Reactive Oxygen Species (ROS) derived from mitochondrial respiration are frequently cited as a major source of chromosomal DNA mutations that contribute to cancer development and aging. However, experimental evidence showing that ROS released by mitochondria can directly damage nuclear DNA is largely lacking. In this study, we investigated the effects of H 2 O 2 released by mitochondria or produced at the nucleosomes using a titratable chemogenetic approach. This enabled us to precisely investigate to what extent DNA damage occurs downstream of near- and supraphysiological amounts of localized H 2 O 2 . Nuclear H 2 O 2 gives rise to DNA damage and mutations and a subsequent p53 dependent cell cycle arrest. Mitochondrial H 2 O 2 release shows none of these effects, even at levels that are orders of magnitude higher than what mitochondria normally produce. We conclude that H 2 O 2 released from mitochondria is unlikely to directly damage nuclear genomic DNA, limiting its contribution to oncogenic transformation and aging. Nuclear DNA damage downstream of mitochondrial ROS is often cited to contribute to cancer initiation and aging. However, here the authors show that although H 2 O 2 induces DNA mutations when produced near DNA, it does not when released by mitochondria.
AbstractList Abstract Reactive Oxygen Species (ROS) derived from mitochondrial respiration are frequently cited as a major source of chromosomal DNA mutations that contribute to cancer development and aging. However, experimental evidence showing that ROS released by mitochondria can directly damage nuclear DNA is largely lacking. In this study, we investigated the effects of H 2 O 2 released by mitochondria or produced at the nucleosomes using a titratable chemogenetic approach. This enabled us to precisely investigate to what extent DNA damage occurs downstream of near- and supraphysiological amounts of localized H 2 O 2 . Nuclear H 2 O 2 gives rise to DNA damage and mutations and a subsequent p53 dependent cell cycle arrest. Mitochondrial H 2 O 2 release shows none of these effects, even at levels that are orders of magnitude higher than what mitochondria normally produce. We conclude that H 2 O 2 released from mitochondria is unlikely to directly damage nuclear genomic DNA, limiting its contribution to oncogenic transformation and aging.
Reactive Oxygen Species (ROS) derived from mitochondrial respiration are frequently cited as a major source of chromosomal DNA mutations that contribute to cancer development and aging. However, experimental evidence showing that ROS released by mitochondria can directly damage nuclear DNA is largely lacking. In this study, we investigated the effects of H 2 O 2 released by mitochondria or produced at the nucleosomes using a titratable chemogenetic approach. This enabled us to precisely investigate to what extent DNA damage occurs downstream of near- and supraphysiological amounts of localized H 2 O 2 . Nuclear H 2 O 2 gives rise to DNA damage and mutations and a subsequent p53 dependent cell cycle arrest. Mitochondrial H 2 O 2 release shows none of these effects, even at levels that are orders of magnitude higher than what mitochondria normally produce. We conclude that H 2 O 2 released from mitochondria is unlikely to directly damage nuclear genomic DNA, limiting its contribution to oncogenic transformation and aging. Nuclear DNA damage downstream of mitochondrial ROS is often cited to contribute to cancer initiation and aging. However, here the authors show that although H 2 O 2 induces DNA mutations when produced near DNA, it does not when released by mitochondria.
Reactive Oxygen Species (ROS) derived from mitochondrial respiration are frequently cited as a major source of chromosomal DNA mutations that contribute to cancer development and aging. However, experimental evidence showing that ROS released by mitochondria can directly damage nuclear DNA is largely lacking. In this study, we investigated the effects of H2O2 released by mitochondria or produced at the nucleosomes using a titratable chemogenetic approach. This enabled us to precisely investigate to what extent DNA damage occurs downstream of near- and supraphysiological amounts of localized H2O2. Nuclear H2O2 gives rise to DNA damage and mutations and a subsequent p53 dependent cell cycle arrest. Mitochondrial H2O2 release shows none of these effects, even at levels that are orders of magnitude higher than what mitochondria normally produce. We conclude that H2O2 released from mitochondria is unlikely to directly damage nuclear genomic DNA, limiting its contribution to oncogenic transformation and aging.
Abstract Reactive Oxygen Species (ROS) derived from mitochondrial respiration are frequently cited as a major source of chromosomal DNA mutations that contribute to cancer development and aging. However, experimental evidence showing that ROS released by mitochondria can directly damage nuclear DNA is largely lacking. In this study, we investigated the effects of H2O2 released by mitochondria or produced at the nucleosomes using a titratable chemogenetic approach. This enabled us to precisely investigate to what extent DNA damage occurs downstream of near- and supraphysiological amounts of localized H2O2. Nuclear H2O2 gives rise to DNA damage and mutations and a subsequent p53 dependent cell cycle arrest. Mitochondrial H2O2 release shows none of these effects, even at levels that are orders of magnitude higher than what mitochondria normally produce. We conclude that H2O2 released from mitochondria is unlikely to directly damage nuclear genomic DNA, limiting its contribution to oncogenic transformation and aging.
Reactive Oxygen Species (ROS) derived from mitochondrial respiration are frequently cited as a major source of chromosomal DNA mutations that contribute to cancer development and aging. However, experimental evidence showing that ROS released by mitochondria can directly damage nuclear DNA is largely lacking. In this study, we investigated the effects of H2O2 released by mitochondria or produced at the nucleosomes using a titratable chemogenetic approach. This enabled us to precisely investigate to what extent DNA damage occurs downstream of near- and supraphysiological amounts of localized H2O2. Nuclear H2O2 gives rise to DNA damage and mutations and a subsequent p53 dependent cell cycle arrest. Mitochondrial H2O2 release shows none of these effects, even at levels that are orders of magnitude higher than what mitochondria normally produce. We conclude that H2O2 released from mitochondria is unlikely to directly damage nuclear genomic DNA, limiting its contribution to oncogenic transformation and aging.Nuclear DNA damage downstream of mitochondrial ROS is often cited to contribute to cancer initiation and aging. However, here the authors show that although H2O2 induces DNA mutations when produced near DNA, it does not when released by mitochondria.
ArticleNumber 2725
Author Polderman, Paulien E.
den Toom, Wytze T. F.
Zwakenberg, Susan
Lehmann, Johannes
van Boxtel, Ruben
Burgering, Boudewijn M. T.
van Soest, Daan M. K.
Keijer, Janneke P.
van Roosmalen, Markus J.
Leyten, Tim M. F.
De Henau, Sasha
Dansen, Tobias B.
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Snippet Reactive Oxygen Species (ROS) derived from mitochondrial respiration are frequently cited as a major source of chromosomal DNA mutations that contribute to...
Abstract Reactive Oxygen Species (ROS) derived from mitochondrial respiration are frequently cited as a major source of chromosomal DNA mutations that...
Abstract Reactive Oxygen Species (ROS) derived from mitochondrial respiration are frequently cited as a major source of chromosomal DNA mutations that...
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Cancer
Cell cycle
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Deoxyribonucleic acid
DNA
DNA damage
Humanities and Social Sciences
Hydrogen peroxide
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multidisciplinary
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Reactive oxygen species
Science
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Title Mitochondrial H2O2 release does not directly cause damage to chromosomal DNA
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