Linked Life Data

2009525

Source:http://linkedlifedata.com/resource/pubmed/id/2009525

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
1991-5-7
pubmed:abstractText
F-344 rats fed diets containing phenethyl isothiocyanate (PEITC; 3 and 6 mumol/g diet), a naturally occurring constituent of cruciferous vegetables, before and during treatment with the carcinogen N-nitrosobenzylmethylamine (NBMA), developed 99-100% fewer esophageal tumors than NBMA-treated control rats. PEITC exhibited inhibitory effects against both preneoplastic lesions (acanthosis and hyperkeratosis, leukoplakia, leukokeratosis) and neoplastic lesions (papilloma, carcinoma). Tumors were not observed in rats treated with PEITC alone. The effects of PEITC (10, 25, 50, 100 microM) on the metabolism and DNA binding of NBMA in cultured explants of rat esophagus were also investigated. PEITC produced a marked (53-97%) dose-dependent inhibition in the binding of NBMA metabolites to DNA and in the levels of DNA methylation at the N7 (20-89%) and O6 (55-93%) positions of guanine. This isothiocyanate also reduced the metabolism of NBMA by esophageal tissues as indicated by increased amounts of unmetabolized NBMA in the medium of cultures containing PEITC. Collectively, these data indicate that PEITC is a potent inhibitor of NBMA-induced esophageal carcinogenesis in rats.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0008-5472
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
51
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2063-8
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Inhibitory effects of phenethyl isothiocyanate on N-nitrosobenzylmethylamine carcinogenesis in the rat esophagus.
pubmed:affiliation
Department of Pathology, Medical College of Ohio, Toledo 43614.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.