| pubmed-article:10535996 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10535996 | lifeskim:mentions | umls-concept:C0030493 | lld:lifeskim |
| pubmed-article:10535996 | lifeskim:mentions | umls-concept:C0132555 | lld:lifeskim |
| pubmed-article:10535996 | lifeskim:mentions | umls-concept:C0600688 | lld:lifeskim |
| pubmed-article:10535996 | lifeskim:mentions | umls-concept:C1314939 | lld:lifeskim |
| pubmed-article:10535996 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:10535996 | pubmed:issue | 22 | lld:pubmed |
| pubmed-article:10535996 | pubmed:dateCreated | 1999-12-10 | lld:pubmed |
| pubmed-article:10535996 | pubmed:abstractText | Paraquat (PQ) is a well described pneumotoxicant that produces toxicity by redox cycling with cellular diaphorases, thereby elevating intracellular levels of superoxide (O-(2)). NO synthase (NOS) has been shown to participate in PQ-induced lung injury. Current theory holds that NO reacts with O-(2) generated by PQ to produce the toxin peroxynitrite. We asked whether NOS might alternatively function as a PQ diaphorase and reexamined the question of whether NO/O-(2) reactions were toxic or protective. Here, we show that: (i) neuronal NOS has PQ diaphorase activity that inversely correlates with NO formation; (ii) PQ-induced endothelial cell toxicity is attenuated by inhibitors of NOS that prevent NADPH oxidation, but is not attenuated by those that do not; (iii) PQ inhibits endothelium-derived, but not NO-induced, relaxations of aortic rings; and (iv) PQ-induced cytotoxicity is potentiated in cytokine-activated macrophages in a manner that correlates with its ability to block NO formation. These data indicate that NOS is a PQ diaphorase and that toxicity of such redox-active compounds involves a loss of NO-related activity. | lld:pubmed |
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| pubmed-article:10535996 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10535996 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10535996 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:10535996 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10535996 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:10535996 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:10535996 | pubmed:author | pubmed-author:PaterWW | lld:pubmed |
| pubmed-article:10535996 | pubmed:author | pubmed-author:DayB JBJ | lld:pubmed |
| pubmed-article:10535996 | pubmed:author | pubmed-author:ChengP YPY | lld:pubmed |
| pubmed-article:10535996 | pubmed:author | pubmed-author:StamlerJ SJS | lld:pubmed |
| pubmed-article:10535996 | pubmed:author | pubmed-author:CalavettaLL | lld:pubmed |
| pubmed-article:10535996 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10535996 | pubmed:day | 26 | lld:pubmed |
| pubmed-article:10535996 | pubmed:volume | 96 | lld:pubmed |
| pubmed-article:10535996 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10535996 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10535996 | pubmed:pagination | 12760-5 | lld:pubmed |
| pubmed-article:10535996 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:10535996 | pubmed:meshHeading | pubmed-meshheading:10535996... | lld:pubmed |
| pubmed-article:10535996 | pubmed:year | 1999 | lld:pubmed |
| pubmed-article:10535996 | pubmed:articleTitle | A mechanism of paraquat toxicity involving nitric oxide synthase. | lld:pubmed |
| pubmed-article:10535996 | pubmed:affiliation | Department of Medicine, National Jewish Medical and Research Center, School of Pharmacy, University of Colorado Health Sciences Center, Denver, CO 80206, USA. DAYB@njc.org | lld:pubmed |
| pubmed-article:10535996 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10535996 | pubmed:publicationType | In Vitro | lld:pubmed |
| pubmed-article:10535996 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:10535996 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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