Linked Life Data

2839405

Source:http://linkedlifedata.com/resource/pubmed/id/2839405

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1988-8-25
pubmed:abstractText
In an attempt to elucidate the role of hepatic macrophages in liver injury, we investigated galactosamine-treated rats (500 mg per kg body weight). The rats received an i.v. injection of latex particles (2 x 10(9) particles per animal) prior to (latex-galactosamine) or 12 to 16 hr subsequent to the galactosamine treatment (galactosamine-latex). Effect of superoxide dismutase on hepatic injury induced by galactosamine or galactosamine-latex treatment was also examined. Oxygen-derived free radical-generating capacity of isolated hepatic macrophages was measured as chemiluminescence with the stimulation of phorbol myristate acetate or latex particles. As compared with normal rats, chemiluminescence of hepatic macrophages from galactosamine-treated rats was 5- to 10-fold enhanced 12 hr following galactosamine treatment and remained elevated for 48 hr. Chemiluminescence of the latex particle-pretreated macrophages in the liver was markedly suppressed even following the galactosamine treatment (p less than 0.01). Compared to galactosamine-treated rats, both lipid peroxide level in the liver tissue and AST and ALT concentration in serum were significantly decreased in the latex-galactosamine-treated rats (p less than 0.01) and increased in the galactosamine-latex-treated rats (p less than 0.01). Furthermore, superoxide dismutase supplementation protected against liver injury induced by the galactosamine-latex treatment. From these results, pretreatment with latex particles suppressed the free radical-generating capacity of hepatic macrophages and protected against hepatic injury induced by galactosamine. In contrast, injection of latex particles after galactosamine treatment aggravated hepatic injury, which was prevented by superoxide dismutase. These data suggest that liver injury induced by galactosamine is modulated by oxygen-derived free radicals from hepatic macrophages.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0270-9139
pubmed:author
pubmed:issnType
Print
pubmed:volume
8
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
815-21
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:2839405-Alanine Transaminase, pubmed-meshheading:2839405-Animals, pubmed-meshheading:2839405-Aspartate Aminotransferases, pubmed-meshheading:2839405-Drug-Induced Liver Injury, pubmed-meshheading:2839405-Galactosamine, pubmed-meshheading:2839405-Latex, pubmed-meshheading:2839405-Lipid Peroxides, pubmed-meshheading:2839405-Lipopolysaccharides, pubmed-meshheading:2839405-Liver, pubmed-meshheading:2839405-Luminescent Measurements, pubmed-meshheading:2839405-Macrophages, pubmed-meshheading:2839405-Male, pubmed-meshheading:2839405-Malondialdehyde, pubmed-meshheading:2839405-Microspheres, pubmed-meshheading:2839405-Rats, pubmed-meshheading:2839405-Rats, Inbred Strains, pubmed-meshheading:2839405-Superoxide Dismutase, pubmed-meshheading:2839405-Superoxides, pubmed-meshheading:2839405-Tetradecanoylphorbol Acetate
pubmed:articleTitle
Modulation of hepatotoxicity by macrophages in the liver.
pubmed:affiliation
Second Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't