| pubmed-article:36434 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:36434 | lifeskim:mentions | umls-concept:C0301896 | lld:lifeskim |
| pubmed-article:36434 | lifeskim:mentions | umls-concept:C0431085 | lld:lifeskim |
| pubmed-article:36434 | lifeskim:mentions | umls-concept:C0184633 | lld:lifeskim |
| pubmed-article:36434 | lifeskim:mentions | umls-concept:C0439857 | lld:lifeskim |
| pubmed-article:36434 | lifeskim:mentions | umls-concept:C0085416 | lld:lifeskim |
| pubmed-article:36434 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:36434 | pubmed:dateCreated | 1979-9-1 | lld:pubmed |
| pubmed-article:36434 | pubmed:abstractText | Experiments were done to determine 1) whether the respiratory burst of superoxide anion (O2-) production in polymorphonuclear leukocytes (PMN) is triggered during antibody-dependent killing of tumor cells and 2) whether O2- production is essential for cytotoxicity. Three parameters of the respiratory burst (1-14C-glucose oxidation, oxygen consumption, and O2- release) were increased 2.5- to 7.3-fold during killing of antibody-primed tumor cells by human PMN. Added catalase and superoxide dismutase did not inhibit lysis, possibly because these enzymes were unable to diffuse into the inter-plasma-membrane space between killer and target cells. Evidence for an O2- requirement for cytotoxicity was the fact that concentrations of amobarbital or phenylbutazone sufficient to inhibit the cyanide-insensitive respiration of PMN also inhibited cytotoxicity. Also, hypoxic conditions inhibited cytotoxicity from 29 to 73%. The requirement for oxygen was most likely related to O2- generation and not mitochondrial respiration since cyanide and azide, which inhibit mitochondrial respiration, increased cytotoxicity. | lld:pubmed |
| pubmed-article:36434 | pubmed:language | eng | lld:pubmed |
| pubmed-article:36434 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:36434 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:36434 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:36434 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:36434 | pubmed:issn | 0022-1767 | lld:pubmed |
| pubmed-article:36434 | pubmed:author | pubmed-author:LucasZ JZJ | lld:pubmed |
| pubmed-article:36434 | pubmed:author | pubmed-author:HafemanD GDG | lld:pubmed |
| pubmed-article:36434 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:36434 | pubmed:volume | 123 | lld:pubmed |
| pubmed-article:36434 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:36434 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:36434 | pubmed:pagination | 55-62 | lld:pubmed |
| pubmed-article:36434 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:36434 | pubmed:year | 1979 | lld:pubmed |
| pubmed-article:36434 | pubmed:articleTitle | Polymorphonuclear leukocyte-mediated, antibody-dependent, cellular cytotoxicity against tumor cells: dependence on oxygen and the respiratory burst. | lld:pubmed |
| pubmed-article:36434 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:36434 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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