| pubmed-article:15686116 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15686116 | lifeskim:mentions | umls-concept:C0024554 | lld:lifeskim |
| pubmed-article:15686116 | lifeskim:mentions | umls-concept:C0025925 | lld:lifeskim |
| pubmed-article:15686116 | lifeskim:mentions | umls-concept:C0007022 | lld:lifeskim |
| pubmed-article:15686116 | lifeskim:mentions | umls-concept:C0032403 | lld:lifeskim |
| pubmed-article:15686116 | lifeskim:mentions | umls-concept:C0178602 | lld:lifeskim |
| pubmed-article:15686116 | lifeskim:mentions | umls-concept:C0332293 | lld:lifeskim |
| pubmed-article:15686116 | lifeskim:mentions | umls-concept:C2697585 | lld:lifeskim |
| pubmed-article:15686116 | pubmed:dateCreated | 2005-2-2 | lld:pubmed |
| pubmed-article:15686116 | pubmed:abstractText | Overactivation of poly(ADP-ribose) polymerase-1 (PARP-1) in response to oxidative stress has been shown to contribute to necrotic cell death by consuming NAD+ and ATP. In the present study, PARP-1 overactivation was determined by identifying the distribution and accumulation of poly(ADP-ribose) following intraperitoneal administration of a hepatotoxic dose of carbon tetrachloride (572 mg/kg). Treated animals exhibited lipid peroxide levels 16.5-fold higher than controls. Serum activities of glutamic pyruvic transaminase and glutamic oxaloacetic transaminase were increased by 6.1-fold and 22.8-fold, respectively. Lactate dehydrogenase activity was significantly increased by 1.2-fold. Histopathological analyses revealed severe necrosis and increased poly(ADP-ribsyl)ation of cells in the centrilobular region of treated animals versus saline controls. These results demonstrate the role of PARP-1 overactivation in chemical-induced pathologies and suggest the potential role of PARP-1 inhibitors at preventing toxicity. | lld:pubmed |
| pubmed-article:15686116 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15686116 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15686116 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:15686116 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15686116 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15686116 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15686116 | pubmed:issn | 1078-0297 | lld:pubmed |
| pubmed-article:15686116 | pubmed:author | pubmed-author:TanakaSeigoS | lld:pubmed |
| pubmed-article:15686116 | pubmed:author | pubmed-author:UedaKunihiroK | lld:pubmed |
| pubmed-article:15686116 | pubmed:author | pubmed-author:Muro-CachoCar... | lld:pubmed |
| pubmed-article:15686116 | pubmed:author | pubmed-author:TakehashiMasa... | lld:pubmed |
| pubmed-article:15686116 | pubmed:author | pubmed-author:SuPhi-HuynhPH | lld:pubmed |
| pubmed-article:15686116 | pubmed:author | pubmed-author:HarbisonRaymo... | lld:pubmed |
| pubmed-article:15686116 | pubmed:author | pubmed-author:StedefordTodd... | lld:pubmed |
| pubmed-article:15686116 | pubmed:author | pubmed-author:BanasikMarekM | lld:pubmed |
| pubmed-article:15686116 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15686116 | pubmed:volume | 113-114 | lld:pubmed |
| pubmed-article:15686116 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15686116 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15686116 | pubmed:pagination | 171-9 | lld:pubmed |
| pubmed-article:15686116 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
| pubmed-article:15686116 | pubmed:meshHeading | pubmed-meshheading:15686116... | lld:pubmed |
| pubmed-article:15686116 | pubmed:meshHeading | pubmed-meshheading:15686116... | lld:pubmed |
| pubmed-article:15686116 | pubmed:meshHeading | pubmed-meshheading:15686116... | lld:pubmed |
| pubmed-article:15686116 | pubmed:meshHeading | pubmed-meshheading:15686116... | lld:pubmed |
| pubmed-article:15686116 | pubmed:meshHeading | pubmed-meshheading:15686116... | lld:pubmed |
| pubmed-article:15686116 | pubmed:meshHeading | pubmed-meshheading:15686116... | lld:pubmed |
| pubmed-article:15686116 | pubmed:meshHeading | pubmed-meshheading:15686116... | lld:pubmed |
| pubmed-article:15686116 | pubmed:meshHeading | pubmed-meshheading:15686116... | lld:pubmed |
| pubmed-article:15686116 | pubmed:meshHeading | pubmed-meshheading:15686116... | lld:pubmed |
| pubmed-article:15686116 | pubmed:meshHeading | pubmed-meshheading:15686116... | lld:pubmed |
| pubmed-article:15686116 | pubmed:meshHeading | pubmed-meshheading:15686116... | lld:pubmed |
| pubmed-article:15686116 | pubmed:year | 2003 | lld:pubmed |
| pubmed-article:15686116 | pubmed:articleTitle | Hepatocellular accumulation of poly(ADP-ribose) in male ICR mice treated with a necrogenic dose of carbon tetrachloride. | lld:pubmed |
| pubmed-article:15686116 | pubmed:affiliation | Center for Environmental and Occupational Risk Analysis and Management, Department of Environmental and Occupational Health, College of Public Health, University of South Florida, Tampa, Florida 33612, USA. | lld:pubmed |
| pubmed-article:15686116 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15686116 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
| pubmed-article:15686116 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
