Abstract
We describe the events triggered by a sub-lethal concentration of airborne particulate matter (PM(10)) in A549 cells, which include the formation DNA double-strand breaks, gammaH2A.X generation, and 53BP1 recruitment. To protect the genome, cells activated ATM/ATR/Chk1/Chk2/p53 pathway but, after 48 h, cells turned into a senescence-like state. Trolox, an antioxidant, was able to prevent most of the alterations observed after particulate matter exposure, demonstrating the important role of ROS as mediator of PM(10)-induced genotoxicity and suggesting that DNA damage could be the mechanisms by which particulate matter augment the risk of lung cancer.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Apoptosis
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Ataxia Telangiectasia Mutated Proteins
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Cell Cycle
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Cell Cycle Proteins / analysis
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Cell Line, Tumor
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DNA Breaks, Double-Stranded
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DNA Damage*
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DNA-Binding Proteins / analysis
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Humans
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Particulate Matter / toxicity*
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Protein Serine-Threonine Kinases / analysis
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Reactive Oxygen Species / metabolism
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Tumor Suppressor Protein p53 / physiology
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Tumor Suppressor Proteins / analysis
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cdc25 Phosphatases / analysis
Substances
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Cell Cycle Proteins
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DNA-Binding Proteins
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Particulate Matter
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Reactive Oxygen Species
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Tumor Suppressor Protein p53
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Tumor Suppressor Proteins
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ATM protein, human
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ATR protein, human
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Ataxia Telangiectasia Mutated Proteins
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Protein Serine-Threonine Kinases
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CDC25A protein, human
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cdc25 Phosphatases