Wood smoke particles generate free radicals and cause lipid peroxidation, DNA damage, NFκB activation and TNF-α release in macrophages

Stephen S. Leonard, Suwei Wang, Xianglin Shi, Bryan S. Jordan, Vince Castranova, Michael A. Dubick

Research output: Contribution to journalArticlepeer-review

94 Scopus citations

Abstract

The present study investigated the generation of free radicals by wood smoke and cellular injuries caused by these radicals. Wood smoke was collected after thermolysis of western bark. Electron spin resonance (ESR) techniques were used to measure both carbon-centered radicals and generation of reactive oxygen species (ROS) by wood smoke. Wood smoke, in the presence of H2O2, was found to be able to generate hydroxyl radical (·OH). DNA strand breakage was measured by exposing wood smoke to λ Hind III fragments using gel electrophoresis. Wood smoke combined with H2O2 caused DNA damage. Sodium formate, an ·OH radical scavenger, or deferoxamine, a metal chelator, inhibited the DNA damage. Cellular DNA damage was also measured in cultured RAW 264.7 mouse macrophage cells by the single cell gel (SCG) electrophoresis assay. Cells were exposed to wood smoke samples for various times and significant DNA damage was observed. Elemental analysis was performed on the filter samples and the presence of Fe was noteworthy. Wood smoke is also able to cause lipid peroxidation, activate nuclear transcription factor, NFκB, and enhance the release of TNF-α from RAW 264.7 cells. The results indicate that the free radicals generated by wood smoke through the reaction of Fe with H2O2 are able to cause DNA and cellular damage and may act as a fibrogenic agent. (C) 2000 Elsevier Science Ireland Ltd.

Original languageEnglish
Pages (from-to)147-157
Number of pages11
JournalToxicology
Volume150
Issue number1-3
DOIs
StatePublished - Sep 7 2000

Keywords

  • DNA damage
  • Free radicals
  • Wood smoke

ASJC Scopus subject areas

  • Toxicology

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