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Oxidative stress mediates air pollution particle-induced acute lung injury and molecular pathology

Elizabeth S Roberts1, Judy H Richards, Richard Jaskot

  • 1Department of Molecular Biomedical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, North Carolina, USA.

Inhalation Toxicology
|October 22, 2003
PubMed

Insights

Ambient air particulate matter (PM) causes lung injury through oxidative stress. Dimethylthiourea (DMTU) pretreatment protected against oil combustion particle-induced lung inflammation and molecular pathology in rats.

Area of Science:

  • Environmental Health
  • Toxicology
  • Pulmonary Medicine

Background:

  • Epidemiological studies link ambient air particulate matter (PM) to increased morbidity and mortality.
  • In vitro studies offer mechanistic insights but extrapolation to in vivo lung injury is challenging.
  • Understanding in vivo mechanisms of PM-induced lung injury is crucial for biological plausibility.

Purpose of the Study:

  • To investigate the in vivo mechanisms of lung injury induced by oil combustion particles.
  • To evaluate the role of oxidative stress in particulate matter-induced lung pathology.
  • To assess the protective effects of dimethylthiourea (DMTU) against particulate matter-induced lung injury.

Main Methods:

  • Rats were pretreated with dimethylthiourea (DMTU) before intratracheal instillation of residual oil fly ash (ROFA).
  • Bronchoalveolar lavage was performed to assess biomarkers of lung injury.
  • Immunohistochemical, biochemical, and molecular approaches were used to analyze lung tissues for signaling pathway alterations and gene expression.

Main Results:

  • Residual oil fly ash (ROFA) exposure led to significant pulmonary inflammation, cytotoxicity, and activation of ERK mitogen-activated protein kinase (MAPK).
  • ROFA increased mRNA levels of inflammatory mediators including macrophage inflammatory protein (MIP)-2, interleukin (IL)-6, tumor necrosis factor (TNF)-alpha, MCP-1, and matrilysin.
  • Dimethylthiourea (DMTU) pretreatment significantly inhibited ROFA-induced inflammation, cytotoxicity, ERK MAPK activation, and inflammatory gene expression.

Conclusions:

  • Oxidative stress plays a critical role in residual oil fly ash (ROFA)-induced lung injury and associated molecular pathology.
  • Findings demonstrate a direct extrapolation from in vitro to in vivo particulate matter (PM) mechanistic information.
  • Dimethylthiourea (DMTU) effectively mitigates particulate matter-induced lung injury, highlighting the importance of targeting oxidative stress.

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