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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。
Objective To investigate the induction of CYP1A1 and aromatase receptor (AHR) mRNA by 2,3,7,8-tetrachlorodibenzo-p-thcoxetine (TCDD) in the liver of SD rats and to explore its toxic mechanism. Methods Thirty female Sprague-Dawley rats were randomly divided into control group and five exposure groups, with 5 in each group. The exposure doses were 0.010, 10.01, 10.0, 10.0, μg TCDD / kg body weight. The cells were injected intraperitoneally once. After 24 h, the induction of CYP1A1 and AHR mRNA in the liver was measured by RT-PCR. Results In addition to 0.1 μg TCDD / kg body weight, AHR and CYP1A1 mRNA expressions were increased in all exposure groups. AHR mRNA was significantly increased at 50 μg TCDD / kg body weight (P <0.05) , CYP1A1mRNA significantly increased in all treatment groups except0.0μg / kg body weight, the difference was significant (P <0.05), and there was a dose-effect relationship between the dose and AHR and CYP1A1mRNA relationship. Conclusions TCDD can induce the expression of AHR and CYP1A1 in liver of SD rats 24 h after exposure, and CYP1A1 is more easily induced than AHR.