||Breakage and Binding of DNA by Reaction Products of Hypochlorous Acid with Aniline, 1-Napthylamine, or 1-Naphthol.
Kozumbo, W. J. ;
Agarwal, S. ;
Koren, H. S. ;
||North Carolina Univ. at Chapel Hill. Center for Environmental Medicine and Lung Biology.;Health Effects Research Lab., Research Triangle Park, NC.;National Institutes of Health, Bethesda, MD.
DNA damage ;
Deoxyribonucleic acids ;
Hypochlorous acids ;
Binding sites ;
In vitro analysis ;
Ultraviolet spectrophotometry ;
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Inhaled tobacco smoke and urban smog can elicit inflammatory neutrophils into the lung. They also contain aryl compounds absorbed to particles which, when phagocytized by neutrophils or monocytes trigger intraphagosomal and extracellular release of hypochlorous acid (HOC1), a potently reactive oxidant. Using aniline, 1-naphthylamine and 1-napthol (1-NOH) as model pollutant compounds, we examined whether HOC1 (OC1) could potentially transform phagocytized compounds into genotoxic products. Compounds (15-25 micro M) were first reacted with HOC1 (25-150 micro M) in phosphate buffer and then used to treat diploid human lung fibroblasts or purified DNA. DNA single-strand breaks/alkali-labile sites were assayed in cells by DNA alkaline elution, and binding of HOC1-reacted ((14)C) 1NOH to purified DNA was analyzed by scintillation spectrometry. Neither HOC1 nor compounds alone could break DNA, but HOC1-reacted compounds induced up to 400 red equivalents of DNA damage.