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Asbestos-induced pulmonary toxicity: role of DNA damage and apoptosis

Daya Upadhyay1, David W Kamp

  • 1Division of Pulmonary and Critical Care Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611, USA.

Experimental Biology and Medicine (Maywood, N.J.)
|May 30, 2003
PubMed

Insights

Asbestos exposure causes DNA damage and cell death (apoptosis) through oxidative stress. Strategies to reduce this stress may prevent asbestos-related cancers.

Area of Science:

  • Environmental Toxicology
  • Molecular Biology
  • Cancer Research

Background:

  • Asbestos exposure is linked to lung diseases and cancers, but the precise mechanisms remain unclear.
  • Genotoxicity, including DNA strand breaks and apoptosis, is a key factor in asbestos-induced cellular damage.
  • Oxidative stress, mediated by reactive oxygen species (ROS), is implicated in asbestos-related DNA damage.

Purpose of the Study:

  • To review evidence on asbestos's direct genotoxicity in lung cells.
  • To explore the mechanisms underlying asbestos-induced DNA damage and apoptosis.
  • To highlight the role of oxidative stress and DNA repair pathways.

Main Methods:

  • Review of accumulating scientific evidence on asbestos genotoxicity.
  • Analysis of studies investigating ROS generation and mitochondrial dysfunction.
  • Examination of DNA repair enzyme activation, including APE and PARP.

Main Results:

  • Asbestos directly induces DNA strand breaks and apoptosis in lung target cells.
  • Iron-derived ROS play a significant role in asbestos-induced DNA damage.
  • Asbestos activates DNA repair enzymes, but damage may overwhelm repair capacity.

Conclusions:

  • Asbestos-induced oxidative stress contributes to DNA damage and apoptosis.
  • A persistent proliferative signal combined with overwhelming DNA damage can lead to neoplastic transformation.
  • Targeting asbestos-induced oxidative stress may offer a strategy for cancer prevention.

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