Carlson Erik A, Roy Nirmal K, Wirgin Isaac I
Gulf Coast Research Laboratory, University of Southern Mississippi, 703 East Beach Drive, Ocean Springs, Mississippi 39564, USA.
Environ Toxicol Chem. 2009 Apr;28(4):759-71. doi: 10.1897/08-195R.1.
Several populations of fishes inhabiting contaminated Atlantic Coast estuaries exhibit resistance to early life-stage (ELS) toxicities induced by halogenated aromatic hydrocarbons such as coplanar polychlorinated biphenyls (PCBs). These toxicities include mortality, circulatory failure, edema, and craniofacial malformations. The mechanisms behind resistance to halogenated aromatic hydrocarbon toxicity in these populations are unknown. First and second generation Atlantic tomcod Microgadus tomcod embryos derived from the Hudson River ([HR]; New York, USA) population are highly resistant to PCB-induced cytochrome P4501A (CYP1A) expression and ELS toxicity when compared to embryos of Miramichi River ([MR]; New Brunswick, Canada) and Shinnecock Bay ([SB]; New York, USA) origin. The present study sought to identify novel genes involved in population differences in response to PCB exposure using custom microarrays. Microarray probes consisted of unsequenced inserts of randomly picked clones from a tomcod cardiac cDNA library. Tomcod embryos from three populations (HR, MR, and SB) were exposed to two doses of an environmentally relevant mixture of coplanar PCBs and screened for dose- and population-specific patterns of gene expression. Clones displaying significant differences between populations exposed to the high dose of PCBs were identified by DNA sequencing. Of the 28 identified nonribosomal protein clones, none displayed expression patterns highly similar to CYP1A (altered in MR and SB, but not in HR). However, several transcripts representing biomarkers of cardiomyopathy in mammals (cardiac troponin T2, cathepsin L, and atrial natriuretic peptide) were differentially altered among the three tomcod populations by PCBs. Although the present study did not identify any novel genes associated with PCB resistance in tomcod, several potential molecular biomarkers of PCB exposure were revealed.
栖息在受污染的大西洋海岸河口的几种鱼类种群,对卤代芳烃(如共平面多氯联苯(PCBs))诱导的早期生命阶段(ELS)毒性具有抗性。这些毒性包括死亡率、循环系统衰竭、水肿和颅面畸形。这些种群对卤代芳烃毒性产生抗性的机制尚不清楚。与来自米拉米奇河([MR];加拿大新不伦瑞克省)和申纳科克湾([SB];美国纽约)的胚胎相比,源自哈得逊河([HR];美国纽约)种群的第一代和第二代大西洋小鳕(Microgadus tomcod)胚胎对PCB诱导的细胞色素P4501A(CYP1A)表达和ELS毒性具有高度抗性。本研究试图使用定制微阵列鉴定与对PCB暴露反应的种群差异相关的新基因。微阵列探针由从小鳕心脏cDNA文库中随机挑选的克隆的未测序插入片段组成。来自三个种群(HR、MR和SB)的小鳕胚胎暴露于两种剂量的与环境相关的共平面PCBs混合物中,并筛选基因表达的剂量和种群特异性模式。通过DNA测序鉴定在暴露于高剂量PCBs的种群之间表现出显著差异的克隆。在鉴定出的28个非核糖体蛋白克隆中,没有一个显示出与CYP1A高度相似的表达模式(在MR和SB中改变,但在HR中未改变)。然而,几种代表哺乳动物心肌病生物标志物的转录本(心肌肌钙蛋白T2、组织蛋白酶L和心钠素)在三个小鳕种群中因PCBs而有差异地改变。尽管本研究未鉴定出与小鳕对PCB抗性相关的任何新基因,但揭示了几种潜在的PCB暴露分子生物标志物。