Source:http://linkedlifedata.com/resource/pubmed/id/12649045
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2
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| pubmed:dateCreated |
2003-3-21
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| pubmed:abstractText |
Line A, B, and C rats were selectively bred from TCDD-resistant Han/Wistar (Kuopio; H/W) and TCDD-sensitive Long-Evans (Turku/AB; L-E) rats. Line A rats are the most resistant to TCDD acute lethality followed by line B and line C rats. The resistance in line A rats is associated with a mutated H/W-type aryl hydrocarbon receptor (Ahr) allele (Ahr(hw)) and in line B rats the resistance is associated with an allele of an unknown gene B (B(hw)), while line C rats are almost as sensitive to TCDD as L-E rats. The dose-responses of characteristic short-term effects (day 8 postexposure) of TCDD were used to evaluate the efficacy (magnitude of effect) and potency relationships between these lines. Line A rats showed similar efficacies as line C (line A:line C efficacy ratio more than 0.7) for thymus weight, EROD activity, and incisor tooth defects. In contrast, efficacies in line A were decreased (efficacy ratios 0.19-0.37) for body weight change, serum bilirubin, and FFA levels, and serum ASAT activity. For most endpoints the efficacies in line B rats seem to be lower than in line C rats. The potencies were close to each other in line A and B rats, but somewhat lower than in line C rats. The results support our previous concept of two different AHR-mediated signaling pathways leading to dioxin type I and type II endpoints. Rats with the Ahr(hw/hw) genotype show a markedly decreased efficacy for type II endpoints, but B(hw) allele had only a minor effect on efficacies for most endpoints. Both H/W-type resistance alleles also decreased the potency of TCDD. However, the potency differences in short-term toxicity seem not to explain, at least alone, the differences seen in acute lethality among the rat lines.
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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/Aspartate Aminotransferases,
http://linkedlifedata.com/resource/pubmed/chemical/Bilirubin,
http://linkedlifedata.com/resource/pubmed/chemical/Cytochrome P-450 CYP1A1,
http://linkedlifedata.com/resource/pubmed/chemical/Fatty Acids, Nonesterified,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Aryl Hydrocarbon,
http://linkedlifedata.com/resource/pubmed/chemical/Tetrachlorodibenzodioxin
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| pubmed:status |
MEDLINE
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| pubmed:month |
Mar
|
| pubmed:issn |
0041-008X
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| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
1
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| pubmed:volume |
187
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| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
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| pubmed:pagination |
128-36
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| pubmed:dateRevised |
2006-11-15
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| pubmed:meshHeading |
pubmed-meshheading:12649045-Alleles,
pubmed-meshheading:12649045-Animals,
pubmed-meshheading:12649045-Aspartate Aminotransferases,
pubmed-meshheading:12649045-Bilirubin,
pubmed-meshheading:12649045-Body Weight,
pubmed-meshheading:12649045-Crosses, Genetic,
pubmed-meshheading:12649045-Cytochrome P-450 CYP1A1,
pubmed-meshheading:12649045-Fatty Acids, Nonesterified,
pubmed-meshheading:12649045-Female,
pubmed-meshheading:12649045-Genetic Predisposition to Disease,
pubmed-meshheading:12649045-Incisor,
pubmed-meshheading:12649045-Liver,
pubmed-meshheading:12649045-Organ Size,
pubmed-meshheading:12649045-Rats,
pubmed-meshheading:12649045-Rats, Long-Evans,
pubmed-meshheading:12649045-Rats, Wistar,
pubmed-meshheading:12649045-Receptors, Aryl Hydrocarbon,
pubmed-meshheading:12649045-Tetrachlorodibenzodioxin,
pubmed-meshheading:12649045-Thymus Gland
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| pubmed:year |
2003
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| pubmed:articleTitle |
Dose-response analysis of short-term effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin in three differentially susceptible rat lines.
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| pubmed:affiliation |
National Public Health Institute, Department of Environmental Health, P.O. Box 95, FIN-70701 Kuopio, Finland. ulla.simanainen@ktl.fi
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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