Pedlar R M, Ptashynski M D, Evans R, Klaverkamp J F
Department of Zoology, University of Manitoba, Winnipeg, MB, Canada R3T 2N2.
Aquat Toxicol. 2002 May;57(3):167-89. doi: 10.1016/s0166-445x(01)00198-9.
Adult lake whitefish were fed As contaminated diets at nominal concentrations of 0, 1, 10, and 100 microg As/g food (dry weight) for 10, 30, and 64 days. Reduced feed consumption was observed in lake whitefish fed the 100 microg As/g food, beginning on day 45 of exposure. The accumulation and distribution of As in these fish are described in the previous manuscript [Pedlar, R.M., Klaverkamp, J.F., 2001. The accumulation and distribution of dietary arsenic in lake whitefish (Coregonus clupeaformis). Aquat. Toxicol., in press]. At the molecular level of organization, metallothionein (MT) induction occurred in lake whitefish fed the 100 microg As/g food after 10 and 30 days, and in fish fed the 1 and 10 microg As/g diets for 64 days. Dietary As exposure did not have a significant effect on plasma lipid peroxide (LPO) concentrations. At the tissue and organ level, mean liver somatic index decreased significantly in lake whitefish fed the 100 microg As/g food for 64 days. Blood parameters (hematocrit, hemoglobin concentration, red blood cell count, mean cell volume, mean corpuscular hemoglobin, and mean corpuscular hemoglobin concentration) were not affected by exposure to As contaminated diets. Liver and gallbladder histopathologies were observed in lake whitefish fed all As contaminated diets after each duration of exposure. Histopathology observed in liver included nuclear, architectural and structural alterations, areas of inflammation, and focal necrosis. Sloughing of the epithelium, dilation of vascular elements, inflammation, edema, fibrosis, and increased width of the submucosa were some of the alterations observed in gallbladders of lake whitefish fed As contaminated diets. Both organs were sensitive to As exposure, as damage occurred with exposure to dietary concentrations of As as low as 1 microg/g. Whole organism parameters were unaltered by dietary As exposure. Based on the results of this study, histopathological alterations in liver and gallbladder, and hepatic MT induction may be useful indicators of As toxicity in environmental monitoring programs that also measure As concentrations in those tissues.
成年湖白鲑被投喂了标称浓度分别为0、1、10和100微克砷/克食物(干重)的砷污染饲料,投喂时间分别为10天、30天和64天。从暴露第45天开始,观察到投喂100微克砷/克食物的湖白鲑饲料消耗量减少。这些鱼体内砷的积累和分布情况在之前的手稿中已有描述[佩德lar,R.M.,克拉弗坎普,J.F.,2001年。湖白鲑(Coregonus clupeaformis)膳食砷的积累和分布。水生毒理学,即将发表]。在组织分子水平上,投喂100微克砷/克食物的湖白鲑在10天和30天后出现金属硫蛋白(MT)诱导,投喂1和10微克砷/克饲料64天的鱼也出现MT诱导。膳食砷暴露对血浆脂质过氧化物(LPO)浓度没有显著影响。在组织和器官水平上,投喂100微克砷/克食物64天的湖白鲑肝脏体指数显著下降。血液参数(血细胞比容、血红蛋白浓度、红细胞计数、平均细胞体积、平均红细胞血红蛋白含量和平均红细胞血红蛋白浓度)不受砷污染饲料暴露的影响。在每个暴露时间段后,观察到投喂所有砷污染饲料的湖白鲑肝脏和胆囊出现组织病理学变化。在肝脏中观察到的组织病理学变化包括细胞核、结构和构造改变、炎症区域和局灶性坏死。投喂砷污染饲料的湖白鲑胆囊出现的变化包括上皮脱落、血管扩张、炎症、水肿、纤维化和黏膜下层增宽。这两个器官对砷暴露都很敏感,因为在膳食砷浓度低至1微克/克时就会出现损伤。膳食砷暴露未改变整个生物体的参数。基于本研究结果,肝脏和胆囊的组织病理学变化以及肝脏MT诱导可能是环境监测项目中砷毒性的有用指标,这些项目还会测量这些组织中的砷浓度。