Linked Life Data

18350280

Source:http://linkedlifedata.com/resource/pubmed/id/18350280

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2008-8-4
pubmed:abstractText
Carcinogenic risk and molecular mechanisms underlying the liver tumor-promoting activity of copper gluconate, an additive of functional foods, were investigated using a rat medium-term liver carcinogenicity bioassay protocol (Ito test) and a 2-week short-term administration experiment. In the medium-term liver bioassay, Fischer 344 male rats were given a single i.p. injection of N-nitrosodiethylamine at a dose of 200 mg/kg b.w. as a carcinogenic initiator. Starting 2 weeks thereafter, rats received 0, 10, 300 or 6,000 ppm of copper gluconate in diet for 6 weeks. All rats underwent 2/3 partial hepatectomy at the end of week 3, and all surviving rats were killed at the end of week 8. In the short-term experiment, rats were given 0, 10, 300 or 6,000 ppm of copper gluconate for 2 weeks. Numbers of glutathione S-transferase placental form (GST-P) positive lesions, single GST-P-positive hepatocytes and 8-oxoguanine-positive hepatocytes, and levels of cell proliferation and apoptosis in the liver were significantly increased by 6,000 ppm of copper gluconate in the medium-term liver bioassay. Furthermore, hepatic mRNA expression of genes relating to the metal metabolism, inflammation and apoptosis were elevated by 6,000 ppm of copper gluconate both in the medium-term liver bioassay and the short-term experiments. These results indicate that copper gluconate possesses carcinogenic risk toward the liver at the high dose level, and that oxidative stress and inflammatory and pro-apoptotic signaling statuses may participate in its underlying mechanisms.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0340-5761
pubmed:author
pubmed:issnType
Print
pubmed:volume
82
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
563-71
pubmed:meshHeading
pubmed-meshheading:18350280-Administration, Oral, pubmed-meshheading:18350280-Animals, pubmed-meshheading:18350280-Apoptosis, pubmed-meshheading:18350280-Biological Assay, pubmed-meshheading:18350280-Carcinogenicity Tests, pubmed-meshheading:18350280-Carcinogens, pubmed-meshheading:18350280-Cell Proliferation, pubmed-meshheading:18350280-Diet, pubmed-meshheading:18350280-Dose-Response Relationship, Drug, pubmed-meshheading:18350280-Gene Expression Profiling, pubmed-meshheading:18350280-Gene Expression Regulation, Neoplastic, pubmed-meshheading:18350280-Gluconates, pubmed-meshheading:18350280-Glutathione Transferase, pubmed-meshheading:18350280-Guanine, pubmed-meshheading:18350280-Hepatectomy, pubmed-meshheading:18350280-Hepatocytes, pubmed-meshheading:18350280-Liver, pubmed-meshheading:18350280-Liver Neoplasms, pubmed-meshheading:18350280-Male, pubmed-meshheading:18350280-Metallothionein, pubmed-meshheading:18350280-Metals, pubmed-meshheading:18350280-Oxidative Stress, pubmed-meshheading:18350280-Precancerous Conditions, pubmed-meshheading:18350280-RNA, Messenger, pubmed-meshheading:18350280-Rats, pubmed-meshheading:18350280-Rats, Inbred F344
pubmed:year
2008
pubmed:articleTitle
Carcinogenic risk of copper gluconate evaluated by a rat medium-term liver carcinogenicity bioassay protocol.
pubmed:affiliation
Toxicology and Environmental Science Department, Biological Research Laboratories, Nissan Chemical Industries Limited, Saitama, Japan. abem@nissanchem.co.jp
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't