Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1995-6-15
pubmed:abstractText
Exposure to hyperoxia causes alveolar macrophage (AM) injury. The present study investigates the roles of intracellular antioxidant enzymes and of glutathione in the protection of AMs against hyperoxia in a biphasic cell culture system in aerobiosis. The effect of normoxia or hyperoxia on the integrity of AMs was related to indices of cell injury (ATP cell content and lactate dehydrogenase release into culture medium) and cell mass (protein content of AMs). Antioxidant activities were measured in guinea-pig AMs exposed to 95% O2 or to normoxia (control cells) for 3 days. A 3-day AM culture in normoxia showed a significant decrease in protein and catalase, whereas ATP cell content, superoxide dismutase (SOD) (both Cu,Zn-SOD and Mn-SOD) and glutathione peroxidase (GPx) activities significantly increased. The content of reduced glutathione (GSH) did not change. Using the ATP content in AMs expressed as a cell injury index (CII), AM injury increased with increasing O2 exposure time (1 day: 13 +/- 4.4%; 2 days: 34 +/- 3.8%; 3 days: 40 +/- 4.1%; 4 days: 55 +/- 7.3%; 6 days: 87.5 +/- 5.4%). Exposure to 95% O2 for 3 days was associated with a significant decrease in ATP cell content, protein, catalase and GSH to the total glutathione ratio, whereas SOD, GSH and total glutathione did not change significantly. The GPx activities increased significantly. There was no significant correlation between the AM CII and SOD or GPx content. In contrast, a significant correlation was observed between hyperoxia-induced AM CII and catalase content (r = 0.71) and glutathione content (r = 0.71).(ABSTRACT TRUNCATED AT 250 WORDS)
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0260-437X
pubmed:author
pubmed:issnType
Print
pubmed:volume
15
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
53-8
pubmed:dateRevised
2003-11-14
pubmed:meshHeading
pubmed-meshheading:7745227-Adenosine Triphosphate, pubmed-meshheading:7745227-Aerobiosis, pubmed-meshheading:7745227-Animals, pubmed-meshheading:7745227-Antimetabolites, pubmed-meshheading:7745227-Buthionine Sulfoximine, pubmed-meshheading:7745227-Catalase, pubmed-meshheading:7745227-Cell Survival, pubmed-meshheading:7745227-Cells, Cultured, pubmed-meshheading:7745227-Drug Interactions, pubmed-meshheading:7745227-Glutamate-Cysteine Ligase, pubmed-meshheading:7745227-Glutathione Peroxidase, pubmed-meshheading:7745227-Guinea Pigs, pubmed-meshheading:7745227-Hyperoxia, pubmed-meshheading:7745227-L-Lactate Dehydrogenase, pubmed-meshheading:7745227-Macrophages, Alveolar, pubmed-meshheading:7745227-Methionine Sulfoximine, pubmed-meshheading:7745227-Microscopy, Electron, Scanning, pubmed-meshheading:7745227-Proteins, pubmed-meshheading:7745227-Superoxide Dismutase
pubmed:articleTitle
Relationship between oxygen-induced alveolar macrophage injury and cell antioxidant defence.
pubmed:affiliation
Laboratoire de Pathologie Respiratoire Expérimentale et de Pollution Atmosphérique, Lille, France.
pubmed:publicationType
Journal Article