Linked Life Data

3206528

Source:http://linkedlifedata.com/resource/pubmed/id/3206528

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1989-2-3
pubmed:abstractText
Male B6C3F1 mice, 6 weeks of age, were fed diets or water containing di(2-ethylhexyl) phthalate (DEHP) at 12,000 or 6000 ppm, acetaminophen (ACT) at 10,000 or 5000 ppm, sodium barbital (BBS) at 1000 ppm, or phenobarbital (PB) at 500 ppm for 40 weeks. Groups of six mice were terminated at 2, 8, 24, and 40 weeks for evaluation of liver and kidney weights, histopathology, and thymidine kinase (TK) activity in liver and kidney and levels of DNA synthesis, measured by tritiated thymidine [( 3H]T) autoradiography or bromodeoxyuridine (BrdU) immunohistochemistry. Liver weights, as percentage of body weight, were significantly elevated at most time intervals for mice exposed to all chemicals at each dose. The hepatocyte labeling indices (LI) with [3H]T autoradiography or BrdU immunocytochemistry were significantly elevated in mice fed DEHP at 12,000 ppm at 24 and 40 weeks or BBS and ACT at 2 weeks. LI were not elevated in mice fed PB. Hepatic TK activity was significantly elevated in mice fed DEHP, BBS, or ACT at Weeks 2 and 8. Histopathologic hepatic lesions were associated with these elevations, while hepatic lesions were not associated with changes in TK activity in PB-treated mice. In contrast, only DEHP and BBS induced toxic renal lesions. Persistent or transient elevation of the renal LI and TK activity accompanied renal toxicity. Thus, the hepatic toxin DEHP induced chronic renal hyperplasia without evidence of renal carcinogenicity or tumor promotion in previous studies at the doses used. ACT, a hepatotoxin, produced transient chronic hepatic hyperplasia without evidence of carcinogenicity in B6C3F1 mice in earlier studies at the same doses used. Thus, persistent or transient hepatic or renal hyperplasia was associated with carcinogenic or tumor promoting activity of these chemicals in some cases but not in others.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0041-008X
pubmed:author
pubmed:issnType
Print
pubmed:volume
96
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
494-506
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1988
pubmed:articleTitle
The chronic hepatic or renal toxicity of di(2-ethylhexyl) phthalate, acetaminophen, sodium barbital, and phenobarbital in male B6C3F1 mice: autoradiographic, immunohistochemical, and biochemical evidence for levels of DNA synthesis not associated with carcinogenesis or tumor promotion.
pubmed:affiliation
Division of Cancer Etiology, National Cancer Institute, Frederick, Maryland 21701-1013.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't