Source:http://linkedlifedata.com/resource/pubmed/id/18172886
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rdf:type | |
lifeskim:mentions |
umls-concept:C0005052,
umls-concept:C0015780,
umls-concept:C0017262,
umls-concept:C0017431,
umls-concept:C0023884,
umls-concept:C0026809,
umls-concept:C0039635,
umls-concept:C0080194,
umls-concept:C0205280,
umls-concept:C0332293,
umls-concept:C1337112,
umls-concept:C1511660,
umls-concept:C1553039,
umls-concept:C1705241,
umls-concept:C1705242
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pubmed:issue |
6
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pubmed:dateCreated |
2008-7-28
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pubmed:abstractText |
To search for genes whose products modify aryl hydrocarbon receptor (AhR)-dependent toxicity caused by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), gene expression profiles in the liver were surveyed using microarrays 24 h after the administration of TCDD to three strains of female mice, BALB/cAnN (BALB), C3H/HeN (C3H) and CBA/JN (CBA) all of identical AhR genotype. The BALB/cAnN strain had a more marked induction of a number of glutathione S-transferase (GST) sub-families, particularly the GSTmicro gene family, compared with the other two strains. To assess the effects of GSTs induction to metabolize carcinogens, TCDD (40 microg kg(-1)) was administered to BALB and CBA strains, followed 24 h later by an i.p. injection of low or high dose of benzo[a]pyrene (B[a]P, 50 or 200 mg kg(-1)). The 32P-postlabelling analysis showed that administration of TCDD alone failed to induce DNA adduct formation in both BALB and CBA strain mouse livers. The low dose of B[a]P alone produced DNA adduct in the liver of both strains to a similar extent. Treatment with TCDD 24 h before the low dose of B[a]P suppressed the formation of B[a]P-induced DNA-adduct more markedly in the BALB strain compared with the CBA strain. Taken together, these findings show that TCDD treatment causes strain-specific alterations in gene expression and B[a]P-induced DNA adduct formation in the liver of female mice of the same AhRb2 genotype. Furthermore, it suggests that TCDD-treated female mice of the BALB strain may have genes whose products modify the toxicity of B[a]P as evidenced by TCDD-induced alterations in B[a]P-DNA adduct formation.
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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/Benzo(a)pyrene,
http://linkedlifedata.com/resource/pubmed/chemical/DNA Adducts,
http://linkedlifedata.com/resource/pubmed/chemical/DNA Primers,
http://linkedlifedata.com/resource/pubmed/chemical/Environmental Pollutants,
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 |
Aug
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pubmed:issn |
0260-437X
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pubmed:author | |
pubmed:copyrightInfo |
Copyright 2008 John Wiley & Sons, Ltd.
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pubmed:issnType |
Print
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pubmed:volume |
28
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
724-33
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pubmed:meshHeading |
pubmed-meshheading:18172886-Animals,
pubmed-meshheading:18172886-Benzo(a)pyrene,
pubmed-meshheading:18172886-DNA Adducts,
pubmed-meshheading:18172886-DNA Primers,
pubmed-meshheading:18172886-Environmental Pollutants,
pubmed-meshheading:18172886-Female,
pubmed-meshheading:18172886-Gene Expression,
pubmed-meshheading:18172886-Genotype,
pubmed-meshheading:18172886-Liver,
pubmed-meshheading:18172886-Mice,
pubmed-meshheading:18172886-Mice, Inbred BALB C,
pubmed-meshheading:18172886-Mice, Inbred C3H,
pubmed-meshheading:18172886-Mice, Inbred CBA,
pubmed-meshheading:18172886-Oligonucleotide Array Sequence Analysis,
pubmed-meshheading:18172886-Receptors, Aryl Hydrocarbon,
pubmed-meshheading:18172886-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:18172886-Species Specificity,
pubmed-meshheading:18172886-Tetrachlorodibenzodioxin
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pubmed:year |
2008
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pubmed:articleTitle |
Differences in gene expression and benzo[a]pyrene-induced DNA adduct formation in the liver of three strains of female mice with identical AhRb2 genotype treated with 2,3,7,8-tetrachlorodibenzo-p-dioxin and/or benzo[a]pyrene.
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pubmed:affiliation |
School of Public Health, Fudan University, 130 Dongan Road, Shanghai 200032, China.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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