Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
1992-9-16
pubmed:abstractText
In this study we demonstrate that chloroform, a widely used industrial solvent, a medicinal chemical and a common drinking water contaminant, reduces the number of detectable preneoplastic enzyme-altered foci [gamma-glutamyltranspeptidase-positive (GGT+) and placental form glutathione S-transferase-positive (GST-P+)] in the liver of male Fischer 344 rats. The animals were given a partial hepatectomy and 18 h later received a single oral dose of either 0.5 mmol/kg diethylnitrosamine (DENA) or saline. Two weeks later, groups of 12 animals were started on drinking water containing phenobarbital with varying concentrations (200-1800 mg/l) of chloroform fro 12 weeks. Treated and control animals were killed and the number and the volume of GGT+ and GST-P+ expressing hepatic foci were tabulated. The numbers of foci per unit volume (and per unit area), the percent focal volume and the focal liver were reduced by chloroform in a dose-dependent manner. The mean focal volume was not influenced by chloroform. A plausible explanation for these results could be that chloroform exerts its focal inhibitory effect either by selectively killing the putative initiated cells, by retarding the inherent growth rate of enzyme-altered cells or by reducing the effectiveness of the promoter, phenobarbital. The available evidence suggests that the first hypothesis is the most likely explanation for these observations. These results are consistent with earlier studies showing that chloroform inhibits tumorigenesis in rodents.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0143-3334
pubmed:author
pubmed:issnType
Print
pubmed:volume
13
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1325-30
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:1354081-Analysis of Variance, pubmed-meshheading:1354081-Animals, pubmed-meshheading:1354081-Body Weight, pubmed-meshheading:1354081-Chloroform, pubmed-meshheading:1354081-Cytochrome P-450 CYP1A1, pubmed-meshheading:1354081-Cytochrome P-450 CYP2B1, pubmed-meshheading:1354081-Cytochrome P-450 Enzyme System, pubmed-meshheading:1354081-Diethylnitrosamine, pubmed-meshheading:1354081-Dose-Response Relationship, Drug, pubmed-meshheading:1354081-Drinking, pubmed-meshheading:1354081-Glutathione Transferase, pubmed-meshheading:1354081-Humans, pubmed-meshheading:1354081-Liver, pubmed-meshheading:1354081-Male, pubmed-meshheading:1354081-Microsomes, Liver, pubmed-meshheading:1354081-Organ Size, pubmed-meshheading:1354081-Oxidoreductases, pubmed-meshheading:1354081-Phenobarbital, pubmed-meshheading:1354081-Rats, pubmed-meshheading:1354081-Rats, Inbred F344, pubmed-meshheading:1354081-gamma-Glutamyltransferase
pubmed:year
1992
pubmed:articleTitle
Chloroform inhibits the development of diethylnitrosamine-initiated, phenobarbital-promoted gamma-glutamyltranspeptidase and placental form glutathione S-transferase-positive foci in rat liver.
pubmed:affiliation
US Environmental Protection Agency, Environmental Monitoring Systems Laboratory, Cincinnati, OH 45268.
pubmed:publicationType
Journal Article