Linked Life Data

10828277

Source:http://linkedlifedata.com/resource/pubmed/id/10828277

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2000-7-11
pubmed:abstractText
Bacterial endotoxin (lipopolysaccharide; LPS) given to animals in large doses results in pronounced, midzonal liver injury. Exposure to smaller, non-injurious doses of LPS augments the toxicity of certain hepatotoxicants. This study was conducted to delineate the development of injury in a rat model of augmentation of aflatoxin B(1) (AFB(1)) hepatotoxicity by LPS. At large doses (i.e., > 1 mg/kg, ip), AFB(1) administration resulted in pronounced injury to the periportal regions of the liver. Male, Sprague-Dawley rats (250-350 g) were treated with 1 mg AFB(1)/kg, ip or its vehicle (0.5% DMSO/saline) and 4 h later with either E. coli LPS (7.4 x 106 EU/kg, iv) or its saline vehicle. Liver injury was assessed 6, 12, 24, 48, 72, or 96 h after AFB(1) administration. Hepatic parenchymal cell injury was evaluated as increased alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities in serum and from histologic examination of liver sections. Biliary tract alterations were evaluated as increased concentration of serum bile acids and activities of gamma-glutamyltransferase (GGT), alkaline phosphatase (ALP), and 5'-nucleotidase (5'-ND) in serum. At all times and for all markers, injury in rats treated with either AFB(1) or LPS alone was absent or modest. In the AFB(1)/LPS cotreated group, hepatic parenchymal cell injury was pronounced by 24 h and had returned to control values by 72 h. The injury began in the periportal region and spread midzonally with time. Furthermore, changes in serum markers indicative of biliary tract alterations were evident by 12 h and had returned to control values by 72 h. Thus, the nature of the hepatic lesions suggested that LPS potentiated the effects of AFB(1) on both parenchymal and bile duct epithelial cells.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1096-6080
pubmed:author
pubmed:issnType
Print
pubmed:volume
55
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
444-52
pubmed:dateRevised
2010-9-17
pubmed:meshHeading
pubmed-meshheading:10828277-5'-Nucleotidase, pubmed-meshheading:10828277-Aflatoxin B1, pubmed-meshheading:10828277-Alanine Transaminase, pubmed-meshheading:10828277-Alkaline Phosphatase, pubmed-meshheading:10828277-Animals, pubmed-meshheading:10828277-Apoptosis, pubmed-meshheading:10828277-Aspartate Aminotransferases, pubmed-meshheading:10828277-Bile Acids and Salts, pubmed-meshheading:10828277-Cholestasis, pubmed-meshheading:10828277-Drug Synergism, pubmed-meshheading:10828277-Drug-Induced Liver Injury, pubmed-meshheading:10828277-Escherichia coli, pubmed-meshheading:10828277-In Situ Nick-End Labeling, pubmed-meshheading:10828277-Lipopolysaccharides, pubmed-meshheading:10828277-Liver, pubmed-meshheading:10828277-Male, pubmed-meshheading:10828277-Rats, pubmed-meshheading:10828277-Rats, Sprague-Dawley, pubmed-meshheading:10828277-gamma-Glutamyltransferase
pubmed:year
2000
pubmed:articleTitle
Bacterial lipopolysaccharide exposure augments aflatoxin B(1)-induced liver injury.
pubmed:affiliation
Department of Pharmacology and Toxicology, National Center for Food Safety and Toxicology and Institute for Environmental Toxicology, Michigan State University, East Lansing, Michigan 48824, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.