Source:http://linkedlifedata.com/resource/pubmed/id/18056438
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
23
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pubmed:dateCreated |
2007-12-6
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pubmed:abstractText |
CYP2E1 metabolizes many low-molecular weight toxins and carcinogens. Some in vitro experiments suggest that CYP2E1 may be involved in the metabolic activation of diethylnitrosamine. However, there has been no direct evidence demonstrating a role for CYP2E1 in diethylnitrosamine-mediated carcinogenesis in vivo. To clarify this, we carried out a diethylnitrosamine-induced hepatocarcinogenesis experiment using Cyp2e1-null mice. Male 14-day-old wild-type and Cyp2e1-null mice were treated with diethylnitrosamine (10 mg/kg of body weight) and killed at weeks 24 and 36 after diethylnitrosamine treatment for investigation of tumors and at 6, 24, and 48 h for examination of apoptosis and gene expression. Liver weights of Cyp2e1-null mice were significantly different at weeks 24 and 36 compared with wild-type mice (P < 0.01). Liver tumor incidences of Cyp2e1-null mice were significantly decreased at weeks 24 and 36 compared with wild-type mice (P < 0.01). Cyp2e1-null mice showed significant decrease in the multiplicities of hepatocellular adenoma at weeks 24 and 36 (P < 0.05 and P < 0.01, respectively), and of hepatocellular carcinoma at week 36 (P < 0.01) compared with wild-type mice. Apoptotic index and caspase-3 and/or Bax mRNA expression of Cyp2e1-null mice were significantly different at 6, 24, and 48 h after diethylnitrosamine treatment compared with wild-type mice (P < 0.05). We conclude that Cyp2e1-null mice show lower tumor incidence and multiplicity compared with wild-type mice in diethylnitrosamine-induced hepatocarcinogenesis. It is suggested that CYP2E1 completely participates in diethylnitrosamine-induced hepatocarcinogenesis, and high frequency of tumors in wild-type mice could be associated with the increased apoptosis.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Carcinogens,
http://linkedlifedata.com/resource/pubmed/chemical/Caspase 3,
http://linkedlifedata.com/resource/pubmed/chemical/Cytochrome P-450 CYP2E1,
http://linkedlifedata.com/resource/pubmed/chemical/Diethylnitrosamine,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/bcl-2-Associated X Protein
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
1538-7445
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:day |
1
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pubmed:volume |
67
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
11141-6
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pubmed:meshHeading |
pubmed-meshheading:18056438-Animals,
pubmed-meshheading:18056438-Apoptosis,
pubmed-meshheading:18056438-Blotting, Western,
pubmed-meshheading:18056438-Carcinogens,
pubmed-meshheading:18056438-Carcinoma, Hepatocellular,
pubmed-meshheading:18056438-Caspase 3,
pubmed-meshheading:18056438-Cytochrome P-450 CYP2E1,
pubmed-meshheading:18056438-Diethylnitrosamine,
pubmed-meshheading:18056438-Genotype,
pubmed-meshheading:18056438-Liver Neoplasms, Experimental,
pubmed-meshheading:18056438-Male,
pubmed-meshheading:18056438-Mice,
pubmed-meshheading:18056438-Mice, Inbred C57BL,
pubmed-meshheading:18056438-Mice, Knockout,
pubmed-meshheading:18056438-RNA, Messenger,
pubmed-meshheading:18056438-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:18056438-bcl-2-Associated X Protein
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pubmed:year |
2007
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pubmed:articleTitle |
Role of CYP2E1 in diethylnitrosamine-induced hepatocarcinogenesis in vivo.
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pubmed:affiliation |
Department of Pathology, Osaka City University Medical School, Osaka, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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