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Effects of ozone exposure on lipid metabolism in human alveolar macrophages

Journal Article · · Environmental Health Perspectives; (United States)
DOI:https://doi.org/10.1289/ehp.929795· OSTI ID:6792949
; ;  [1];  [2]
  1. Univ. of North Carolina, Chapel Hill, NC (United States)
  2. Environmental Protection Agency, Research Triangle Park, NC (United States)

Alveolar macrophages (AM) store arachidonic acid (AA), which is esterified in cellular phospholipids until liberated by phospholipase A[sub C] or C after exposure to inflammatory stimuli. After release, there can be subsequent metabolism of AA into various potent, biologically active mediators including prostaglandins and platelet-activating factor (PAF). To examine the possibility that these mediators may account for some of the pathophysiologic alterations seen in the lung after ozone (O[sub 3]) exposure, human AM were collected by bronchoalveolar lavage of normal subjects, plated into tissue culture dishes, and the adherent cells were incubated with [[sup 3]H]AA or [[sup 3]H]lysoPAF. Human AM exposed to 1.0 ppm O[sub 3] for 2 hr released 65 [+-] 12% more tritium, derived from [[sup 3]H]AA, than paired, air-exposed controls into media supernatants. In other studies using a similar O[sub 3] exposure protocol, there was also a significant increase in human AM prostaglandin E[sub 2] production (2.0 [+-] 0.5-fold increase above air-exposure values, p < 0.02, n = 5). These potent lipid mediators, originally derived from human AM, may play an important role in the mechanisms of O[sub 3] lung toxicity. 25 refs., 2 figs., 5 tabs.

OSTI ID:
6792949
Journal Information:
Environmental Health Perspectives; (United States), Journal Name: Environmental Health Perspectives; (United States) Vol. 97; ISSN EVHPAZ; ISSN 0091-6765
Country of Publication:
United States
Language:
English