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首页> 外文期刊>Journal of applied toxicology >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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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.

机译：2,3,7,8-四氯二苯并-对-二恶英和/或苯并（a）处理的三只具有相同AhRb2基因型的雌性小鼠的肝脏中基因表达和苯并（a）induced诱导的DNA加合物形成的差异.。

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摘要

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.
机译：为了寻找其产物修饰由2,3,7,8-四氯二苯并-p-二恶英（TCDD）引起的芳烃受体（AhR）依赖性毒性的基因，在给药后24小时使用微阵列调查了肝脏中的基因表达谱。 TCDD对三种雌性小鼠，BALB / cAnN（BALB），C3H / HeN（C3H）和CBA / JN（CBA）都具有相同的AhR基因型。与其他两个菌株相比，BALB / cAnN菌株对许多谷胱甘肽S-转移酶（GST）亚家族，特别是GSTmicro基因家族的诱导更为明显。为了评估GSTs诱导代谢致癌物的作用，将TCDD（40 microg kg（-1））施用给BALB和CBA菌株，随后24 h腹膜内注射。注射低剂量或高剂量的苯并[a] py（B [a] P，50或200 mg kg（-1））。 32P标记后分析表明，单独使用TCDD无法在BALB和CBA品系小鼠肝脏中诱导DNA加合物形成。单独的低剂量B [a] P在两种菌株的肝脏中都产生了类似的DNA加合物。与CBA菌株相比，在低剂量B [a] P之前24小时用TCDD处理可以更明显地抑制BALB菌株中B [a] P诱导的DNA加合物的形成。综上所述，这些发现表明，TCDD处理可导致具有相同AhRb2基因型的雌性小鼠肝脏中基因表达的特定菌株变化和B [a] P诱导的DNA加合物形成。此外，它暗示了用TCDD处理的BALB株雌性小鼠可能具有其产物修饰B [a] P毒性的基因，如TCDD诱导的B [a] P-DNA加合物形成改变所证明。

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