| pubmed-article:12757849 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12757849 | lifeskim:mentions | umls-concept:C0022646 | lld:lifeskim |
| pubmed-article:12757849 | lifeskim:mentions | umls-concept:C0242606 | lld:lifeskim |
| pubmed-article:12757849 | lifeskim:mentions | umls-concept:C0032829 | lld:lifeskim |
| pubmed-article:12757849 | lifeskim:mentions | umls-concept:C1415619 | lld:lifeskim |
| pubmed-article:12757849 | lifeskim:mentions | umls-concept:C0599946 | lld:lifeskim |
| pubmed-article:12757849 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:12757849 | lifeskim:mentions | umls-concept:C1883709 | lld:lifeskim |
| pubmed-article:12757849 | pubmed:issue | 11 | lld:pubmed |
| pubmed-article:12757849 | pubmed:dateCreated | 2003-5-21 | lld:pubmed |
| pubmed-article:12757849 | pubmed:abstractText | Heme oxygenase (HO) is the rate-limiting enzyme in the degradation of heme; its inducible isozyme HO-1 protects against some types of acute tissue injury. The expression and functional role of HO-1 in rats with renal injury induced by potassium dichromate (K(2)Cr(2)O(7)) was investigated in this work. Rats were studied 24 h after a single injection of K(2)Cr(2)O(7). To address the possible protective effect of HO-1 in this experimental model, this enzyme was induced by an injection of stannous chloride (SnCl(2)) 12 h before K(2)Cr(2)O(7) administration. The functional role of HO-1 in K(2)Cr(2)O(7) + SnCl(2)-treated animals was tested by inhibiting HO activity with an injection of zinc (II) protoporphyrin IX (ZnPP) 18 h before K(2)Cr(2)O(7). In K(2)Cr(2)O(7)-treated rats: (i) renal HO-1 content, measured by Western blot, increased 2.6-fold; and, (ii) renal nitrotyrosine and protein carbonyl content, markers of oxidative stress, increased 3.5- and 1.36-fold, respectively. Renal damage and oxidative stress were ameliorated and HO-1 content was increased in the K(2)Cr(2)O(7) + SnCl(2) group. The attenuation of renal injury and oxidative stress was lost by the inhibition of HO activity in K(2)Cr(2)O(7) + SnCl(2) + ZnPP-treated animals. Our data suggest that HO-1 overexpression induced by SnCl(2) is responsible for the attenuation of renal damage and oxidative stress induced by K(2)Cr(2)O(7). | lld:pubmed |
| pubmed-article:12757849 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12757849 | pubmed:language | eng | lld:pubmed |
| pubmed-article:12757849 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12757849 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:12757849 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12757849 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:12757849 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12757849 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12757849 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12757849 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12757849 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12757849 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12757849 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12757849 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12757849 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12757849 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:12757849 | pubmed:issn | 0891-5849 | lld:pubmed |
| pubmed-article:12757849 | pubmed:author | pubmed-author:Hernández-Pan... | lld:pubmed |
| pubmed-article:12757849 | pubmed:author | pubmed-author:BarreraDianaD | lld:pubmed |
| pubmed-article:12757849 | pubmed:author | pubmed-author:Pedraza-Chave... | lld:pubmed |
| pubmed-article:12757849 | pubmed:author | pubmed-author:MaldonadoPerl... | lld:pubmed |
| pubmed-article:12757849 | pubmed:author | pubmed-author:Medina-Campos... | lld:pubmed |
| pubmed-article:12757849 | pubmed:author | pubmed-author:Ibarra-RubioM... | lld:pubmed |
| pubmed-article:12757849 | pubmed:author | pubmed-author:Pedraza-Chave... | lld:pubmed |
| pubmed-article:12757849 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12757849 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:12757849 | pubmed:volume | 34 | lld:pubmed |
| pubmed-article:12757849 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12757849 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12757849 | pubmed:pagination | 1390-8 | lld:pubmed |
| pubmed-article:12757849 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:12757849 | pubmed:meshHeading | pubmed-meshheading:12757849... | lld:pubmed |
| pubmed-article:12757849 | pubmed:year | 2003 | lld:pubmed |
| pubmed-article:12757849 | pubmed:articleTitle | HO-1 induction attenuates renal damage and oxidative stress induced by K2Cr2O7. | lld:pubmed |
| pubmed-article:12757849 | pubmed:affiliation | Department of Biology, School of Chemistry, Universidad Nacional Autónoma de México, Ciudad Universitaria, 04510 Mexico City, Mexico. | lld:pubmed |
| pubmed-article:12757849 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12757849 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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