Oxygen radicals, inflammation, and tissue injury
dc.contributor.author | Ward, Peter A. | en_US |
dc.contributor.author | Warren, Jeffrey S. | en_US |
dc.contributor.author | Johnson, Kent J. | en_US |
dc.date.accessioned | 2006-04-07T20:32:15Z | |
dc.date.available | 2006-04-07T20:32:15Z | |
dc.date.issued | 1988 | en_US |
dc.identifier.citation | Ward, Peter A., Warren, Jeffrey S., Johnson, Kent J. (1988)."Oxygen radicals, inflammation, and tissue injury." Free Radical Biology and Medicine 5(5-6): 403-408. <http://hdl.handle.net/2027.42/27560> | en_US |
dc.identifier.uri | http://www.sciencedirect.com/science/article/B6T38-47P8D1W-6G/2/7d42b62c0551bcb0f1ba6dd45eec8f67 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/27560 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=3076883&dopt=citation | en_US |
dc.description.abstract | Inflammatory reactions often result in the activation and recruitment of phagocytic cells (e.g., neutrophils and/ or tissue macrophages) whose products result in injury to the tissue. In killing of endothelial cells by activated neutrophils as well as in lung injury produced by either activated neutrophils or activated macrophages there is evidence that H2O2 and iron play a role. HO[middle dot] may be a key oxygen product related to the process of injury. Endothelial cells in some vascular compartments may be susceptible to neutrophil mediated injury in a manner that is independent of oxygen radicals. On the basis of in vitro observations, a synergy exits between platelets and neutrophils, resulting in enhanced oxygen radical formation by the latter. Finally, the cytokines, interleukin 1 and tumor necrosis factor, released from macrophages have both direct stimulatory effects on oxygen radical formation in neutrophils and can "prime" macrophages for enhanced oxygen radical responses to other agonists. Cytokines may also alter endothelial cells rendering them more susceptible to oxygen radical mediated injury by neutrophils. This suggests a complex network of interactions between phagocytic cells and peptide mediators, the result of which is acute, oxygen radical mediated tissue injury. | en_US |
dc.format.extent | 621807 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, inflammation, and tissue 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 | vDepartment of Pathology, The University of Michigan Medical School, M5240 Medical Science I, Box 0602, 1301 Catherine Road, Ann Arbor, MI 48109-0602, U.S.A. | en_US |
dc.contributor.affiliationum | Department of Pathology, The University of Michigan Medical School, M5240 Medical Science I, Box 0602, 1301 Catherine Road, Ann Arbor, MI 48109-0602, U.S.A. | en_US |
dc.contributor.affiliationum | Department of Pathology, The University of Michigan Medical School, M5240 Medical Science I, Box 0602, 1301 Catherine Road, Ann Arbor, MI 48109-0602, U.S.A. | en_US |
dc.identifier.pmid | 3076883 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/27560/1/0000604.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1016/0891-5849(88)90114-1 | en_US |
dc.identifier.source | Free Radical Biology and Medicine | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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