Wood smoke particles generate free radicals and cause lipid peroxidation, DNA damage, NFkappaB activation and TNF-alpha release in macrophages.
Leonard-SS; Wang-S; Shi-X; Jordan-BS; Castranova-V; Dubick-MA
Toxicology 2000 Sep; 150(1-3):147-157
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 H(2)O(2), was found to be able to generate hydroxyl radical (OH). DNA strand breakage was measured by exposing wood smoke to lambda Hind III fragments using gel electrophoresis. Wood smoke combined with H(2)O(2) 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, NFkappaB, and enhance the release of TNF-alpha from RAW 264. 7 cells. The results indicate that the free radicals generated by wood smoke through the reaction of Fe with H(2)O(2) are able to cause DNA and cellular damage and may act as a fibrogenic agent.
Wood-dusts; Peroxides; Injuries; Sodium-compounds; Chelates; Chelating-agents; Exposure-assessment; Iron-compounds; Fibrogenesis; Fibrogenicity
Pathology and Physiology Research Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, M/S 2015, 1095 Willowdale Road, Morgantown, WV 26505, USA