NDLI: Differences in gene expression and benzo[a]pyrene-induced DNA adduct formation in the liver of three strains of female mice with identical $AhR^{b2}$ genotype treated with 2,3,7,8-tetrachlorodibenzo-p-dioxin and/or benzo[a]pyrene

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Differences in gene expression and benzo[a]pyrene-induced DNA adduct formation in the liver of three strains of female mice with identical $AhR^{b2}$ genotype treated with 2,3,7,8-tetrachlorodibenzo-p-dioxin and/or benzo[a]pyrene

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Differences in gene expression and benzo[a]pyrene-induced DNA adduct formation in the liver of three strains of female mice with identical $AhR^{b2}$ genotype treated with 2,3,7,8-tetrachlorodibenzo-p-dioxin and/or benzo[a]pyrene

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Wu, Qing Suzuki, Junko S. Zaha, Hiroko Lin, Tien-Min Peterson, Richard E. Tohyama, Chiharu Ohsako, Seiichiroh
Description	Country affiliation: China Author Affiliation: Wu Q ( School of Public Health, Fudan University, 130 Dongan Road, Shanghai 200032, China.)
Abstract	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 GSTmu gene family, compared with the other two strains. To assess the effects of GSTs induction to metabolize carcinogens, TCDD (40 µg $kg^{−1})$ 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 $^{32}P-postlabelling$ 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 $AhR^{b2}$ 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. Copyright © 2008 John Wiley & Sons, Ltd.
File Format	HTM / HTML
ISSN	0260437X
Issue Number	6
Volume Number	28
e-ISSN	10991263
Journal	Journal of Applied Toxicology
Language	English
Publisher	Wiley
Publisher Date	2008-08-01
Publisher Place	Great Britain (UK)
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Toxicology Benzo(a)pyrene Toxicity Dna Adducts Drug Effects Environmental Pollutants Liver Metabolism Receptors, Aryl Hydrocarbon Genetics Animals Dna Primers Female Gene Expression Genotype Mice Mice, Inbred Balb C Mice, Inbred C3h Mice, Inbred Cba Oligonucleotide Array Sequence Analysis Reverse Transcriptase Polymerase Chain Reaction Species Specificity Journal Article Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Toxicology

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