Overexpression of extracellular superoxide dismutase decreases lung injury after exposure to oil fly ash

Andrew J. Ghio, Hagir B. Suliman, Jacqueline D. Carter, Amir M. Abushamaa, Rodney J. Folz

Research output: Contribution to journalArticlepeer-review

68 Scopus citations


The mechanism of tissue injury after exposure to air pollution particles is not known. The biological effect has been postulated to be mediated via an oxidative stress catalyzed by metals present in particulate matter (PM). We utilized a transgenic (Tg) mouse model that overexpresses extracellular superoxide dismutase (EC-SOD) to test the hypothesis that lung injury after exposure to PM results from an oxidative stress in the lower respiratory tract. Wild-type (Wt) and Tg mice were intratracheally instilled with either saline or 50 μg of residual oil fly ash (ROFA). Twenty-four hours later, specimens were obtained and included bronchoalveolar lavage (BAL) and lung for both homogenization and light histopathology. After ROFA exposure, EC-SOD Tg mice showed a significant reduction in BAL total cell counts (composed primarily of neutrophils) and BAL total protein compared with Wt. ECSOD animals also demonstrated diminished concentrations of inflammatory mediators in BAL. There was no statistically significant difference in BAL lipid peroxidation; however, EC-SOD mice had lower concentrations of oxidized glutathione in the BAL. We conclude that enhanced EC-SOD expression decreased both lung inflammation and damage after exposure to ROFA. This supports a participation of oxidative stress in the inflammatory injury after PM exposure rather than reflecting a response to metals alone.

Original languageEnglish (US)
Pages (from-to)L211-L218
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Issue number1 27-1
StatePublished - 2002


  • Free radicals
  • Particles
  • Transgenic mice
  • Vanadium

ASJC Scopus subject areas

  • Physiology
  • Pulmonary and Respiratory Medicine
  • Physiology (medical)
  • Cell Biology


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