| pubmed-article:9169465 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9169465 | lifeskim:mentions | umls-concept:C0018557 | lld:lifeskim |
| pubmed-article:9169465 | lifeskim:mentions | umls-concept:C0016030 | lld:lifeskim |
| pubmed-article:9169465 | lifeskim:mentions | umls-concept:C0238327 | lld:lifeskim |
| pubmed-article:9169465 | lifeskim:mentions | umls-concept:C0683598 | lld:lifeskim |
| pubmed-article:9169465 | lifeskim:mentions | umls-concept:C0018966 | lld:lifeskim |
| pubmed-article:9169465 | pubmed:issue | 23 | lld:pubmed |
| pubmed-article:9169465 | pubmed:dateCreated | 1997-6-26 | lld:pubmed |
| pubmed-article:9169465 | pubmed:abstractText | The role of heme oxygenase (HO)-1 was evaluated in the oxygen-resistant hamster fibroblast cell line, O2R95, which moderately overexpress HO when compared with the parental cell line, HA-1. To suppress HO-1 expression, O2R95 were transfected with HO-1 antisense oligonucleotide or treated with tin-mesoporphyrin (SnMP). To increase HO-1 expression, cells were transfected with HO-1 cDNA in a pRC/cytomegalovirus (CMV) vector. All cells were challenged with a 48-h exposure to 95% O2 (hyperoxia). When HO activity was suppressed, O2R95 cells had significantly decreased cell viability, increased susceptibility to lipid peroxidation, and increased protein oxidation in hyperoxia. In contrast, further overexpression of HO-1 did not improve resistance to oxygen toxicity. Antisense-transfected cells and SnMP-treated cells with lowered HO activity showed increased levels of cellular heme compared with controls. In the HO-1 cDNA-transfected O2R95 cells, cellular heme was lowered compared with controls; however, cellular redox active iron levels were increased. We conclude that HO mediates cytoprotection to oxygen toxicity within a narrow range of expression. We speculate that this protective effect may be mediated in part through increased metabolism of the pro-oxidant heme but that higher levels of HO activity obviate protection by increased redox active iron release. | lld:pubmed |
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| pubmed-article:9169465 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:9169465 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:9169465 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9169465 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:9169465 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:9169465 | pubmed:author | pubmed-author:LeeC SCS | lld:pubmed |
| pubmed-article:9169465 | pubmed:author | pubmed-author:SpitzD RDR | lld:pubmed |
| pubmed-article:9169465 | pubmed:author | pubmed-author:WongH EHE | lld:pubmed |
| pubmed-article:9169465 | pubmed:author | pubmed-author:RodgersP APA | lld:pubmed |
| pubmed-article:9169465 | pubmed:author | pubmed-author:DenneryP APA | lld:pubmed |
| pubmed-article:9169465 | pubmed:author | pubmed-author:ShokoohiVV | lld:pubmed |
| pubmed-article:9169465 | pubmed:author | pubmed-author:SridharK JKJ | lld:pubmed |
| pubmed-article:9169465 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9169465 | pubmed:day | 6 | lld:pubmed |
| pubmed-article:9169465 | pubmed:volume | 272 | lld:pubmed |
| pubmed-article:9169465 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9169465 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9169465 | pubmed:pagination | 14937-42 | lld:pubmed |
| pubmed-article:9169465 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:9169465 | pubmed:year | 1997 | lld:pubmed |
| pubmed-article:9169465 | pubmed:articleTitle | Heme oxygenase-mediated resistance to oxygen toxicity in hamster fibroblasts. | lld:pubmed |
| pubmed-article:9169465 | pubmed:affiliation | Department of Pediatrics, Stanford University School of Medicine, Stanford, California 94305, USA. mn.phd@forsythe.stanford.edu | lld:pubmed |
| pubmed-article:9169465 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9169465 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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