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Ceruloplasmin inhibits endothelial cell injury and hydroxyl radical production by phorbol myristate acetate (PMA)-stimulated neutrophils

Conference · · FASEB Journal (Federation of American Societies for Experimental Biology); (United States)
OSTI ID:6054102
;  [1]
  1. St. Louis Univ., MO (United States)
Stimulated neutrophils produce oxygen radicals which may cause injury to endothelial cells during inflammatory diseases. Ceruloplasmin is an acute phase protein in which serum levels can increase 2-3 fold during inflammation. Ceruloplasmin may act as an extracellular antioxidant by oxidizing iron and mediating iron-dependent oxygen radical production. The role of ceruloplasmin in reducing injury to endothelial cells and hydroxyl radical production by PMA-stimulated neutrophils was investigated. Ceruloplasmin was purified from human plasma using standard column chromatography methods. Injury to bovine pulmonary using standard column chromatography methods. Injury to bovine pulmonary artery endothelial (BPAE) cells was measured using a {sup 51}chromium release assay. {sub 51}Chromium release from endothelial cells incubated with PMA-stimulated neutrophils was significantly inhibited by 500 {mu}g/ml ceruloplasmin. Hydroxyl radical production by neutrophils was measured using a spectrophotometric deoxyribose degradation assay. Ceruloplasmin at 500 {mu}g/ml significantly stimulated neutrophils. These results indicate that ceruloplasmin may play a role in regulating stimulated neutrophil-mediated endothelial cell injury possibly by preventing the formation of hydroxyl radicals.
OSTI ID:
6054102
Report Number(s):
CONF-9104107--
Conference Information:
Journal Name: FASEB Journal (Federation of American Societies for Experimental Biology); (United States) Journal Volume: 4:3
Country of Publication:
United States
Language:
English

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