| pubmed-article:9559863 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9559863 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:9559863 | lifeskim:mentions | umls-concept:C0596402 | lld:lifeskim |
| pubmed-article:9559863 | lifeskim:mentions | umls-concept:C0020281 | lld:lifeskim |
| pubmed-article:9559863 | lifeskim:mentions | umls-concept:C0525082 | lld:lifeskim |
| pubmed-article:9559863 | lifeskim:mentions | umls-concept:C1511545 | lld:lifeskim |
| pubmed-article:9559863 | lifeskim:mentions | umls-concept:C0136157 | lld:lifeskim |
| pubmed-article:9559863 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:9559863 | pubmed:dateCreated | 1998-6-9 | lld:pubmed |
| pubmed-article:9559863 | pubmed:abstractText | The cytotoxicity of the superoxide anion radical- and nitric oxide-releasing compound SIN-1 to L929 cells was studied in Krebs-Henseleit buffer. pH 7.4, in the presence and absence of Hepes. SIN-1 cytotoxicity was significantly higher in the presence of Hepes than in the absence of Hepes. The available amount of peroxynitrite formed from SIN-1, however, was significantly decreased by Hepes as indicated by decreased oxidation of dihydrorhodamine 123. On the other hand, Hepes largely increased the formation of H2O2 from SIN-1. Catalase protected the L929 cells from SIN-1 cytotoxicity in the buffer with Hepes. In the buffer without Hepes catalase did not have any protective effect. In contrast, tyrosine and tryptophan provided significant protection against SIN-1 cytotoxicity independent of the presence of Hepes. These results demonstrate that the immediate toxic agent formed from SIN-1 decisively depends on the presence of Hepes. In its absence cytotoxicity is most likely mediated by peroxynitrite while in the presence of Hepes, cytotoxicity is conveyed by co-operative action of hydrogen peroxide and reactive nitrogen species. | lld:pubmed |
| pubmed-article:9559863 | pubmed:language | eng | lld:pubmed |
| pubmed-article:9559863 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9559863 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:9559863 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9559863 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9559863 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9559863 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9559863 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9559863 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9559863 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9559863 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9559863 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9559863 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9559863 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:9559863 | pubmed:issn | 0891-5849 | lld:pubmed |
| pubmed-article:9559863 | pubmed:author | pubmed-author:KirschMM | lld:pubmed |
| pubmed-article:9559863 | pubmed:author | pubmed-author:de GrootHH | lld:pubmed |
| pubmed-article:9559863 | pubmed:author | pubmed-author:RauenUU | lld:pubmed |
| pubmed-article:9559863 | pubmed:author | pubmed-author:LomonosovaE... | lld:pubmed |
| pubmed-article:9559863 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9559863 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:9559863 | pubmed:volume | 24 | lld:pubmed |
| pubmed-article:9559863 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9559863 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9559863 | pubmed:pagination | 522-8 | lld:pubmed |
| pubmed-article:9559863 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
| pubmed-article:9559863 | pubmed:meshHeading | pubmed-meshheading:9559863-... | lld:pubmed |
| pubmed-article:9559863 | pubmed:meshHeading | pubmed-meshheading:9559863-... | lld:pubmed |
| pubmed-article:9559863 | pubmed:meshHeading | pubmed-meshheading:9559863-... | lld:pubmed |
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| pubmed-article:9559863 | pubmed:meshHeading | pubmed-meshheading:9559863-... | lld:pubmed |
| pubmed-article:9559863 | pubmed:meshHeading | pubmed-meshheading:9559863-... | lld:pubmed |
| pubmed-article:9559863 | pubmed:meshHeading | pubmed-meshheading:9559863-... | lld:pubmed |
| pubmed-article:9559863 | pubmed:meshHeading | pubmed-meshheading:9559863-... | lld:pubmed |
| pubmed-article:9559863 | pubmed:meshHeading | pubmed-meshheading:9559863-... | lld:pubmed |
| pubmed-article:9559863 | pubmed:meshHeading | pubmed-meshheading:9559863-... | lld:pubmed |
| pubmed-article:9559863 | pubmed:meshHeading | pubmed-meshheading:9559863-... | lld:pubmed |
| pubmed-article:9559863 | pubmed:meshHeading | pubmed-meshheading:9559863-... | lld:pubmed |
| pubmed-article:9559863 | pubmed:meshHeading | pubmed-meshheading:9559863-... | lld:pubmed |
| pubmed-article:9559863 | pubmed:year | 1998 | lld:pubmed |
| pubmed-article:9559863 | pubmed:articleTitle | The critical role of Hepes in SIN-1 cytotoxicity, peroxynitrite versus hydrogen peroxide. | lld:pubmed |
| pubmed-article:9559863 | pubmed:affiliation | Institut für Physiologische Chemie, Universitätsklinikum, Essen, Germany. | lld:pubmed |
| pubmed-article:9559863 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9559863 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
