Linked Life Data

10631129

Source:http://linkedlifedata.com/resource/pubmed/id/10631129

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2000-2-17
pubmed:abstractText
In the previous study we showed that senescent male Fischer 344 rats were resistant to Cd-induced hepatotoxicity compared with young-adult rats. In the present study we investigated the role of Kupffer cells and inflammatory cytokines in this effect of aging. The phagocytic activity of Kupffer cells, determined as the removal of carbon from blood, was stimulated by the administration of a hepatotoxic dose of Cd (3 mg/kg sc) in young-adult (5 months) rats but not in old (28 months) rats. Hepatic concentrations of interleukin (IL)-1beta and cytokine-induced neutrophil chemoattractant (CINC), but not of tumor necrosis factor-alpha or IL-6, were elevated in young rats treated with Cd. In old rats, however, the increase in IL-1beta produced by Cd was not statistically significant and the increase in CINC was much lower than in young-adult rats. Pretreatment with gadolinium chloride or cyclosporin A inhibited the elevations in hepatic cytokines and attenuated Cd-induced liver damage, assessed on the basis of serum alanine aminotransferase and sorbitol dehydrogenase activities. Cd-induced hepatotoxicity in the different treatment groups correlated well with hepatic levels of CINC (r = 0.98, p < 0.001) but not with those of IL-1beta. The results suggest that (1) Kupffer cell activation is essential for inflammatory liver damage from Cd, (2) IL-1beta and CINC are important mediators of the inflammatory response induced by Cd, and (3) the attenuation of Cd-induced liver injury in senescent rats is caused by an impairment in Kupffer cell activation, leading to a lower production of CINC and less inflammatory liver injury.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0041-008X
pubmed:author
pubmed:copyrightInfo
Copyright 2000 Academic Press.
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
162
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
68-75
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:10631129-Age Factors, pubmed-meshheading:10631129-Alanine Transaminase, pubmed-meshheading:10631129-Animals, pubmed-meshheading:10631129-Cadmium, pubmed-meshheading:10631129-Carbon, pubmed-meshheading:10631129-Chemotaxis, pubmed-meshheading:10631129-Cyclosporine, pubmed-meshheading:10631129-Cytokines, pubmed-meshheading:10631129-Dose-Response Relationship, Drug, pubmed-meshheading:10631129-Drug Interactions, pubmed-meshheading:10631129-Drug-Induced Liver Injury, pubmed-meshheading:10631129-Gadolinium, pubmed-meshheading:10631129-Inflammation Mediators, pubmed-meshheading:10631129-Interleukin-1, pubmed-meshheading:10631129-Kupffer Cells, pubmed-meshheading:10631129-L-Iditol 2-Dehydrogenase, pubmed-meshheading:10631129-Male, pubmed-meshheading:10631129-Neutrophil Infiltration, pubmed-meshheading:10631129-Phagocytosis, pubmed-meshheading:10631129-Rats, pubmed-meshheading:10631129-Rats, Inbred F344, pubmed-meshheading:10631129-Time Factors
pubmed:year
2000
pubmed:articleTitle
Attenuation of cadmium-induced liver injury in senescent male fischer 344 rats: role of Kupffer cells and inflammatory cytokines.
pubmed:affiliation
Osaka City Institute of Public Health and Environmental Sciences, Osaka, Japan.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't