Oxygen radicals in complement and neutrophil-mediated acute lung injury
dc.contributor.author | Till, Gerd O. | en_US |
dc.contributor.author | Ward, Peter A. | en_US |
dc.date.accessioned | 2006-04-07T19:13:30Z | |
dc.date.available | 2006-04-07T19:13:30Z | |
dc.date.issued | 1985 | en_US |
dc.identifier.citation | Till, Gerd O., Ward, Peter A. (1985)."Oxygen radicals in complement and neutrophil-mediated acute lung injury." Journal of Free Radicals in Biology & Medicine 1(2): 163-168. <http://hdl.handle.net/2027.42/25857> | en_US |
dc.identifier.uri | http://www.sciencedirect.com/science/article/B73GN-47GGK4H-C/2/b2ae6263c727e229bbd8750a752c0e27 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/25857 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=3915302&dopt=citation | en_US |
dc.description.abstract | The development of experimental acute lung injury following systemic complement activation is closely related to availability of blood neutrophils. Although tissue-destructive neutrophil-derived may play a supportive role in acute pulmonary injury, it appears that oxygen radical constitute the major neutrophil product responsible for acute damage of lung tissues and cells. Intravascular activation of neutrophils by the chemotactic complement peptide C5a is related to the generation os superoxide anion. Dismutation of superoxide to hydrogen peroxide and its iron-mediated conversion to hydroxyl radical appear to constitute in vivo events that ultimately lead to acute lung microvascular injury. | en_US |
dc.format.extent | 577860 bytes | |
dc.format.extent | 3118 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.language.iso | en_US | |
dc.publisher | Elsevier | en_US |
dc.title | Oxygen radicals in complement and neutrophil-mediated acute lung injury | en_US |
dc.type | Article | en_US |
dc.rights.robots | IndexNoFollow | en_US |
dc.subject.hlbsecondlevel | Public Health | en_US |
dc.subject.hlbsecondlevel | Chemistry | en_US |
dc.subject.hlbsecondlevel | Chemical Engineering | en_US |
dc.subject.hlbsecondlevel | Biological Chemistry | en_US |
dc.subject.hlbtoplevel | Engineering | en_US |
dc.subject.hlbtoplevel | Science | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Department of Pathology, The University of Michigan Medical School, Ann Arbor, MI 48109-0010, U.S.A. | en_US |
dc.contributor.affiliationum | Department of Pathology, The University of Michigan Medical School, Ann Arbor, MI 48109-0010, U.S.A. | en_US |
dc.identifier.pmid | 3915302 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/25857/1/0000420.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1016/0748-5514(85)90021-2 | en_US |
dc.identifier.source | Journal of Free Radicals in Biology & Medicine | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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