[2,3,7,8-四氯二苯并对二恶英诱导大鼠肝脏芳烃受体和CYP1A1 mRNA]

[Induction of aryl hydrocarbon receptor and CYP1A1 mRNA by 2,3,7,8-tetrachlorodibenzo-p-dioxin in rat liver].

作者信息

Liu Yun-ru, Tang Nai-jun, Ren Da-lin

机构信息

School of Public Health, Tianjin Medical University, Tianjin 300070, China.

出版信息

Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2003 Dec;21(6):417-9.

PMID:14761350

Abstract

OBJECTIVE

To explore the toxic mechanism of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) by studying the induction of cytochrome P4501A1 (CYP1A1) and aryl hydrocarbon receptor (AHR) mRNA in liver of TCDD-treated SD rats.

METHODS

Thirty female SD rats were randomly divided into control group and 5 exposure groups, every group had 5 rats. The animals were treated i.p. with 0.01, 0.1, 1, 10, 50 microg TCDD/kg BW. AHR and CYP1A1 mRNA expression were analyzed by RT-PCR after 24 h.

RESULTS

The contents of AHR and CYP1A1 mRNA were increased in all exposure groups except the 0.01 microg TCDD/kg BW group. AHR mRNA content was significantly increased in 50 microg TCDD/kg BW group (P<0.05); CYP1A1 mRNA contents were significantly increased in all exposure groups (P<0.05) but not 0.01 microg TCDD/kg BW group. There were dose-response relationship between TCDD doses and AHR, CYP1A1 gene expression.

CONCLUSION

Both AHR and CYP1A1 gene in liver of TCDD-treated SD rats can be induced 24 h after exposure and CYP1A1 gene is more inducible than AHR gene.

摘要

目的

通过研究2,3,7,8-四氯二苯并对二噁英（TCDD）处理的SD大鼠肝脏中细胞色素P4501A1（CYP1A1）和芳烃受体（AHR）mRNA的诱导情况，探讨TCDD的毒性机制。

方法

将30只雌性SD大鼠随机分为对照组和5个染毒组，每组5只。动物经腹腔注射给予0.01、0.1、1、10、50μg TCDD/kg体重。24小时后通过RT-PCR分析AHR和CYP1A1 mRNA表达。

结果

除0.01μg TCDD/kg体重组外，所有染毒组AHR和CYP1A1 mRNA含量均增加。50μg TCDD/kg体重组AHR mRNA含量显著增加（P<0.05）；所有染毒组CYP1A1 mRNA含量均显著增加（P<0.05），但0.01μg TCDD/kg体重组除外。TCDD剂量与AHR、CYP1A1基因表达之间存在剂量-反应关系。