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DNA fragmentation in developing lung fibroblasts exposed to Stachybotrys chartarum (atra) toxins
Author(s) -
McCrae K.C.,
Rand T.G.,
Shaw R.A.,
Mantsch H.H.,
Sowa M.G.,
Thliveris J.A.,
Scott J.E.
Publication year - 2007
Publication title -
pediatric pulmonology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.866
H-Index - 106
eISSN - 1099-0496
pISSN - 8755-6863
DOI - 10.1002/ppul.20608
Subject(s) - dna fragmentation , dna damage , comet assay , fragmentation (computing) , microbiology and biotechnology , biology , dna , chemistry , biochemistry , programmed cell death , apoptosis , ecology
Stachybotrys chartarum (atra) is a toxic mold that grows on water‐damaged cellulose‐based materials. Research has revealed also that inhalation of S. chartarum spores caused marked changes in respiratory epithelium, especially to developing lungs. We analyzed the epigenetic potential of S. chartarum spore toxins on developing rat lung fibroblasts using single cell gel electrophoresis (comet assay). Isolated fetal lung fibroblasts were exposed to S. chartarum spore toxins for 15 min, 3, 14, or 24 hr and control cells were exposed to saline under the same conditions. Cells were embedded in agarose, electrophoresed under alkaline conditions and silver stained. DNA damage was assessed in terms of fragmentation as measured by comet tail length (DNA migration) and intensity (% DNA contained within head and tail). Upon visual inspection, control fibroblasts showed no DNA fragmentation whereas S. chartarum ‐treated cells had definable comets of various degrees depending upon the time‐course. Analyses of the comets revealed that exposure to S. chartarum spore toxins for at least 15 min to 14 hr, induced increased DNA fragmentation in a time‐dependent manner. The fact that exposure to toxins for 24 hr showed less damage suggested that developing lung fibroblasts may have the capability of repairing DNA fragmentation. Pediatr Pulmonol. 2007; 42:592–599. © 2007 Wiley‐Liss, Inc.