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140
Disruption of Yeast Forkhead-associated Cell Cycle Transcription by Oxidative Stress
- Mol. Biol. Cell
"... The effects of oxidative stress on yeast cell cycle depend on the stress-exerting agent. We studied the effects of two oxidative stress agents, hydrogen peroxide (HP) and the superoxide-generating agent Menadione (MD). We found that two small co-expressed groups of genes regulated by the Mcm1-Fkh2-N ..."
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The effects of oxidative stress on yeast cell cycle depend on the stress-exerting agent. We studied the effects of two oxidative stress agents, hydrogen peroxide (HP) and the superoxide-generating agent Menadione (MD). We found that two small co-expressed groups of genes regulated by the Mcm1-Fkh2-Ndd1 transcription regulatory complex are sufficient to account for the difference in the effects of HP and MD on the progress of the cell cycle, namely G1 arrest with MD and an S phase delay followed by a G2/M arrest with HP. Support for this hypothesis is provided by fkh1fkh2 double mutants, which are affected by MD as we find HP affects wild type cells. The apparent involvement of a forkhead protein in HP-induced cell cycle arrest, similar to that reported for C. elegans and human, describes a potentially novel stress-response pathway in yeast.
Werner protein protects nonproliferating cells from oxidative DNA damage
- Mol. Cell Biol
, 2005
"... This article cites 61 articles, 33 of which can be accessed free ..."
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This article cites 61 articles, 33 of which can be accessed free
2004a). Mechanisms of resistance to oxidative and nitrosative stress: implications for fungal survival in mammalian hosts
- Eukaryot Cell
"... This article cites 180 articles, 96 of which can be accessed free ..."
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Cited by 13 (3 self)
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This article cites 180 articles, 96 of which can be accessed free
P: Oxidatively damaged DNA in aging dyslipidemic ApoE -/- and wild-type mice
- Mutagenesis
"... The free radical theory of aging depicts an accumulation of cellular oxidatively damaged DNA. In this study, we investigated this theory in mice with knocked-out apolipo-protein E gene (ApoE2/2), which develops atherosclerosis and wild-type counterparts. The level of oxidatively damaged DNA was inve ..."
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The free radical theory of aging depicts an accumulation of cellular oxidatively damaged DNA. In this study, we investigated this theory in mice with knocked-out apolipo-protein E gene (ApoE2/2), which develops atherosclerosis and wild-type counterparts. The level of oxidatively damaged DNA was investigated as strand breaks, endo-nuclease III- and formamidopyrimidine DNA glycosylase-sensitive sites by the comet assay. The level of DNA damage was mainly increased with age in the liver of ApoE2/2 mice, whereas no increase was observed in the aorta or lung of the mice. This suggests that the accumulation of oxidized DNA in the liver of dyslipidemic ApoE2/2 mice could be secondary to dysfunction of the lipid metabolism. Visually, the aortas of the ApoE2/2 mice were clearly atherosclerotic as indicated by rigid texture and yellowish in color. However, the unaltered levels of oxidized DNA in severely atherosclerotic aortas of old (70 weeks) ApoE2/2 mice indicate that oxidative stress may not be a generalized phenomenon, but rather related locally to the individual plaques. In conclusion, the results of this study suggest that dyslipidemic ApoE2/2 mice suffer from hepatic oxidative stress in terms of oxidized DNA, and this effect could be due to the dysfunction of lipid metabolism.
Futile short-patch DNA base excision repair of adenine:8-oxoguanine mispair
- Nucleic Acids Res
, 2004
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Potential of the dietary antioxidants resveratrol and curcumin in prevention and treatment of hematologic malignancies
- Molecules
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Review Mitochondrial DNA maintenance and bioenergetics
, 2006
"... Oxidative phosphorylation requires assembly of the protein products of both mitochondrial and of nuclear genomes into functional respiratory complexes. Cellular respiration can be compromised when mitochondrial DNA (mtDNA) sequences are corrupted. Oxidative damage resulting from reactive oxygen spec ..."
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Oxidative phosphorylation requires assembly of the protein products of both mitochondrial and of nuclear genomes into functional respiratory complexes. Cellular respiration can be compromised when mitochondrial DNA (mtDNA) sequences are corrupted. Oxidative damage resulting from reactive oxygen species (ROS) produced during respiration is probably a major source of mitochondrial genomic instability leading to respiratory dysfunction. Here, we review mechanisms of mitochondrial ROS production, mtDNA damage and its relationship to mitochondrial dysfunction. We focus particular attention on the roles of mtDNA repair enzymes and processes by which the integrity of the mitochondrial genome is maintained and dysfunction prevented. © 2006 Elsevier B.V. All rights reserved.
Aqueous extracts of the edible Gracilaria tenuistipitata are protective against H2O2-induced DNA damage, growth inhibition, and cell cycle arrest. Molecules 2012
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DAMPs and inflammatory processes: the role of redox in the different outcomes
- Journal of Leukocyte Biology
, 2009
"... Inflammation is deeply entangled with redox modula-tion. Triggering of PRRs on inflammatory cells induces ROS generation. As a consequence, activated cells mount antioxidant responses to counteract the possi-ble harmful effects of oxidation. Therefore, when repair is completed, homeostasis is restor ..."
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Inflammation is deeply entangled with redox modula-tion. Triggering of PRRs on inflammatory cells induces ROS generation. As a consequence, activated cells mount antioxidant responses to counteract the possi-ble harmful effects of oxidation. Therefore, when repair is completed, homeostasis is restored. Here, we de-scribe some recent results showing that an exuberant antioxidant response to pro-oxidant inflammatory stimuli modifies not only the intra- but also the extra-cellular redox and contributes to the outcome of the inflammatory process. In particular, the role of redox modulation in IL-1 secretion, in B lymphocyte differ-entiation to plasma cells, and in tumor progression will be discussed, and the potential consequences of extracellular redox alterations on DAMP activity will be considered. J. Leukoc. Biol. 86: 000–000; 2009.
Cellular repair of oxidatively induced DNA base lesions is defective in prostate cancer cell lines, PC-3 and DU-145
- Carcinogenesis
, 2004
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