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CHEMICAL NATURE AND IMMUNOTOXICOLOGICAL PROPERTIES OF ARACHIDONIC ACID DEGRADATION PRODUCTS FORMED BY EXPOSURE TO OZONE
Citation:
Madden, M., N. Hanley, E. Siegler, J. Quay, S. Becker, R. Devlin, H. Koren, AND M. Friedman. CHEMICAL NATURE AND IMMUNOTOXICOLOGICAL PROPERTIES OF ARACHIDONIC ACID DEGRADATION PRODUCTS FORMED BY EXPOSURE TO OZONE. U.S. Environmental Protection Agency, Washington, D.C., EPA/600/J-95/078.
Description:
Ozone (O3) exposure in vivo has been reported to degrade arachidonic acid (AA) in the lungs of rodents. The O3-degraded AA products may play a role in the lung responses to this toxicant. In order to study the chemical nature and biological activity of O3-exposed AA, we exposed AA in a cell-free, aqueous environment to air, 0.1 ppm, or 1.0 ppm O3 for 15-120 min. AA exposed to air was not degraded. All O3 exposures degraded >98% of the AA to more polar products which were predominantly aldehydic substances (as determined by reactivity with 2,4-dinitrophenylhydrazine and subsequent separation by high performance liquid chromatography) and hydrogen peroxide (H2O2). The type and amount of aldehydic substances formed was dependent on the O3 concentration and exposure duration. When exposed in vitro to 1.0 ppm O3 for 1 hr., a human bronchial epithelial cell line (BEAS-2B, S6 subclone) produced AA-derived aldehydic substances, some of which eluted with similar retention times as the aldehydic substances derived from AA in the cell free system. O3-degraded AA induced an increase in human peripheral blood neutrophil (PMN) polarization, decreased human peripheral blood T-lymphocyte mitogen-stimulated proliferation, and decreased human peripheral blood NK lysis of K562 target cells. The aldehydic substances and not H2O2, appeared to be the principal active agent responsible for the observed effects. O3-degraded AA may play a role in