2,3,7,8-四氯二苯并二噁(口英)对大鼠肝脏芳烃受体和细胞色素P4501A1 mRNA的诱导

目的　研究 2 ,3,7,8 四氯二苯并二口恶 口英 (TCDD)对于SD大鼠肝脏CYP1A1,芳烃受体(AHR)mRNA的诱导 ,探讨其毒作用机制。方法　 30只雌性SD大鼠随机分为对照组和 5个染毒组 ,每组 5只 ,染毒剂量为 0 .0 1、0 .10、1.0 0、10 .0 0、5 0 .0 0 μgTCDD/kg体重 ,用腹腔注射的方式一次染毒 ,2 4h后 ,用RT PCR方法测定肝脏中CYP1A1、AHRmRNA的诱导情况。结果　除 0 .0 1μgTCDD/kg体重外 ,各染毒组AHR和CYP1A1mRNA表达均有所增加 ,其中 ,AHRmRNA在 5 0 μgTCDD/kg体重组明显增加 ,差异有显著性 (P <0 .0 5 ) ,CYP1A1mRNA在除 0 .0 1μgTCDD/kg体重组外的各染毒组明显增加 ,差异均有显著性 (P <0 .0 5 ) ,且染毒剂量与AHR、CYP1A1mRNA诱导之间存在剂量 -效应关系。结论　染毒后 2 4h ,TCDD能诱导SD大鼠肝脏AHR、CYP1A1基因表达 ,CYP1A1基因比AHR基因更容易被诱导。

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

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.