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Effect of the chemical warfare agent, sulfur mustard, on histone H2B serine 14 phosphorylation in primary blood lymphocytes and epithelial cell lines
Author(s) -
Blanton Jason,
Ogidan Olufunso,
Burdette Kristen
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.lb47-c
Subject(s) - sulfur mustard , phosphorylation , serine , histone , microbiology and biotechnology , apoptosis , cell , chromatin , chemistry , biochemistry , biology , dna , toxicity , organic chemistry
The alkylating agent, bis‐(2‐cholroethyl) sulfide (sulfur mustard [SM]), is a vesicant that causes lesions in exposed skin, lungs and eyes. To date, there is no known antidote to either prevent or limit these symptoms. Histones, structural chromatin proteins, are a known target of SM. Examination of the effect of SM on these proteins could provide crucial information about the underlying molecular mechanism of this chemical warfare agent. To that end, we have examined the phosphorylation state of serine 14 of histone H2B in primary blood lymphocytes, human epidermal keratinocytes, bronchial/tracheal epithelial cells and small airway epithelial cells. As serine 14 phosphorylation is a known marker of apoptosis, it seemed probable that SM exposure could lead to phosphorylation at that specific residue. Our results suggest that serine 14 is phosphorylated in primary blood lymphocytes, but not in the other cell types. Preliminary results suggest that the phosphorylation seen in primary blood lymphocytes can be attributed to a known Caspase‐3 pathway. In summary, even though SM exposure is known to result in apoptosis in all cell types tested, there is clearly a cell type difference in the apoptotic pathway used. Determining the cell type specific apoptotic pathways utilized will in turn help in the development of medical countermeasures against chemical warfare agents.