Source:http://linkedlifedata.com/resource/pubmed/id/16089316
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
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| pubmed:dateCreated |
2005-8-10
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| pubmed:abstractText |
Pregnant rats on day 13 of gestation were treated orally with 2 mg/kg of T-2 toxin and sacrificed at 1, 3, 6, 9 and 12 h after the treatment (HAT). Histopathologically, the number of apoptotic cells was increased in the liver, placenta and fetal liver (peaked at 6, 12 and 9-12 HAT, respectively). To examine the gene expression profiles, we performed microarray analysis of these tissues at two selected time points based on the results of the TdT-mediated dUTP nick end labeling (TUNEL) staining. Increased expression of oxidative stress- and apoptosis-related genes was detected in the liver of dams, placenta and fetal liver of pregnant rats treated with T-2 toxin at the peak time point of apoptosis. Decreased expression of lipid metabolism- and drug-metabolizing enzyme-related genes was also detected in these tissues. The results suggested that the mitogen-activated protein kinase (MAPK) pathway might be involved in the mechanism of T-2 toxin-induced apoptosis. In addition, increased expression of the c-jun gene was consistently observed in these tissues. Our results suggest that the mechanism of T-2 toxin-induced toxicity in pregnant rats is due to oxidative stress followed by the activation of the MAPK pathway, finally inducing apoptosis. The c-jun gene may play an important role in T-2 toxin-induced apoptosis.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:month |
Aug
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| pubmed:issn |
0940-2993
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
57
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
15-28
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| pubmed:dateRevised |
2009-11-19
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| pubmed:meshHeading |
pubmed-meshheading:16089316-Administration, Oral,
pubmed-meshheading:16089316-Animals,
pubmed-meshheading:16089316-Apoptosis,
pubmed-meshheading:16089316-Female,
pubmed-meshheading:16089316-Fetus,
pubmed-meshheading:16089316-Gene Expression Profiling,
pubmed-meshheading:16089316-Gene Expression Regulation, Developmental,
pubmed-meshheading:16089316-Genes, jun,
pubmed-meshheading:16089316-In Situ Nick-End Labeling,
pubmed-meshheading:16089316-Liver,
pubmed-meshheading:16089316-Maternal Exposure,
pubmed-meshheading:16089316-Mitogen-Activated Protein Kinases,
pubmed-meshheading:16089316-Oxidative Stress,
pubmed-meshheading:16089316-Placenta,
pubmed-meshheading:16089316-Pregnancy,
pubmed-meshheading:16089316-Protein Array Analysis,
pubmed-meshheading:16089316-RNA, Messenger,
pubmed-meshheading:16089316-Rats,
pubmed-meshheading:16089316-Rats, Wistar,
pubmed-meshheading:16089316-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:16089316-T-2 Toxin
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| pubmed:year |
2005
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| pubmed:articleTitle |
Microarray analysis of T-2 toxin-induced liver, placenta and fetal liver lesions in pregnant rats.
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| pubmed:affiliation |
Medicinal Safety Research Laboratories, Sankyo Co., Ltd., 717 Horikoshi, Fukuroi-shi, Shizuoka 437-0065, Japan. sehata@sankyo.co.jp
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| pubmed:publicationType |
Journal Article
|