DNA damage response of A549 cells treated with particulate matter (PM10) of urban air pollutants

Cancer Lett. 2009 Jun 18;278(2):192-200. doi: 10.1016/j.canlet.2009.01.010. Epub 2009 Feb 13.

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

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis
  • Ataxia Telangiectasia Mutated Proteins
  • Cell Cycle
  • Cell Cycle Proteins / analysis
  • Cell Line, Tumor
  • DNA Breaks, Double-Stranded
  • DNA Damage*
  • DNA-Binding Proteins / analysis
  • Humans
  • Particulate Matter / toxicity*
  • Protein Serine-Threonine Kinases / analysis
  • Reactive Oxygen Species / metabolism
  • Tumor Suppressor Protein p53 / physiology
  • Tumor Suppressor Proteins / analysis
  • cdc25 Phosphatases / analysis

Substances

  • Cell Cycle Proteins
  • DNA-Binding Proteins
  • Particulate Matter
  • Reactive Oxygen Species
  • Tumor Suppressor Protein p53
  • Tumor Suppressor Proteins
  • ATM protein, human
  • ATR protein, human
  • Ataxia Telangiectasia Mutated Proteins
  • Protein Serine-Threonine Kinases
  • CDC25A protein, human
  • cdc25 Phosphatases