Shen Hua, Robertson Larry W, Ludewig Gabriele
Interdisciplinary Graduate Program in Human Toxicology, Graduate College, The University of Iowa, Iowa City, IA, USA.
Department of Occupational & Environmental Health, College of Public Health, The University of Iowa, 100 Oakdale Campus, 214 IREH, Iowa City, IA, 52242-5000, USA.
Environ Sci Pollut Res Int. 2016 Feb;23(3):2108-18. doi: 10.1007/s11356-015-4722-1. Epub 2015 May 27.
Paraoxonase 1 (PON1), an antioxidant enzyme, is believed to play a critical role in many diseases, including cancer. PCBs are widespread environmental contaminants known to induce oxidative stress and cancer and to produce changes in gene expression of various pro-oxidant and antioxidant enzymes. Thus, it appeared of interest to explore whether PCBs may modulate the activity and/or gene expression of PON1 as well. In this study, we compared the effects of dioxin-like and non-dioxin-like PCBs and of various aryl hydrocarbon receptor (AhR) ligands on PON1 regulation and activity in male and female Sprague-Dawley rats. Our results demonstrate that (i) the non-dioxin-like PCB154, PCB155, and PCB184 significantly reduced liver and serum PON1 activities, but only in male rats; (ii) the non-dioxin-like PCB153, the most abundant PCB in many matrices, did not affect PON1 messenger RNA (mRNA) level in the liver but significantly decreased serum PON1 activity in male rats; (iii) PCB126, an AhR ligand and dioxin-like PCB, increased both PON1 activities and gene expression; and (iv) even though three tested AhR ligands induced CYP1A in several tissues to a similar extent, they displayed differential effects on the three PONs and AhR, i.e., PCB126 was an efficacious inducer of PON1, PON2, PON3, and AhR in the liver, while 3-methylcholantrene induced liver AhR and lung PON3, and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), the most potent AhR agonist, increased only PON3 in the lung, at the doses and exposure times used in these studies. These results show that PCBs may have an effect on the antioxidant protection by paraoxonases in exposed populations and that regulation of gene expression through AhR is highly diverse.
对氧磷酶1(PON1)是一种抗氧化酶,被认为在包括癌症在内的多种疾病中起关键作用。多氯联苯是广泛存在的环境污染物,已知其会诱导氧化应激和癌症,并导致各种促氧化酶和抗氧化酶的基因表达发生变化。因此,探讨多氯联苯是否也可能调节PON1的活性和/或基因表达似乎很有意义。在本研究中,我们比较了二噁英类和非二噁英类多氯联苯以及各种芳烃受体(AhR)配体对雄性和雌性Sprague-Dawley大鼠PON1调节和活性的影响。我们的结果表明:(i)非二噁英类多氯联苯PCB154、PCB155和PCB184显著降低了肝脏和血清中的PON1活性,但仅在雄性大鼠中出现;(ii)非二噁英类多氯联苯PCB153是许多基质中含量最高的多氯联苯,它不影响肝脏中PON1信使核糖核酸(mRNA)水平,但显著降低了雄性大鼠血清中的PON1活性;(iii)AhR配体和二噁英类多氯联苯PCB126增加了PON1活性和基因表达;(iv)尽管三种测试的AhR配体在多个组织中诱导CYP1A的程度相似,但它们对三种对氧磷酶和AhR表现出不同的影响,即PCB126是肝脏中PON1、PON2、PON3和AhR的有效诱导剂,而3-甲基胆蒽诱导肝脏AhR和肺PON3,2,3,7,8-四氯二苯并对二噁英(TCDD)是最有效的AhR激动剂,在这些研究中使用的剂量和暴露时间下,仅增加了肺中的PON3。这些结果表明多氯联苯可能对接触人群中对氧磷酶的抗氧化保护产生影响,并且通过AhR对基因表达的调节具有高度多样性。