Examination of the behavior and liver and thyroid histology of juvenile rainbow trout (Oncorhynchus mykiss) exposed to high dietary concentrations of C10-, C11-, C12- and C14-polychlorinated n-alkanes

被引:87
作者
Cooley, HM
Fisk, AT
Wiens, SC
Tomy, GT
Evans, RE
Muir, DCG
机构
[1] Environm Canada, Natl Water Res Inst, Burlington, ON L7R 4A6, Canada
[2] Fisheries & Oceans Canada, Inst Freshwater, Winnipeg, MB R3N 2N6, Canada
[3] Univ Manitoba, Dept Soil Sci, Winnipeg, MB R3T 2N2, Canada
[4] Univ Manitoba, Dept Zool, Winnipeg, MB R3T 2N2, Canada
关键词
chlorinated paraffins; toxicity; fish; narcosis;
D O I
10.1016/S0166-445X(00)00172-7
中图分类号
Q17 [水生生物学];
学科分类号
071004 ;
摘要
Juvenile rainbow trout (Oncorhynchus mykiss) Were exposed to high dietary concentrations of six polychlorinated n-alkane (PCAs) (C10H15.5C6.5, C10H15.5Cl6.5, C10H15.3Cl6.7, C11H18.4Cl5.6, C12H19.5Cl6.5, C14H24.9Cl5.1. and C14H23.3Cl6.7) for 21 to assess their effects on behavior and liver and thyroid histology and for 85 days to assess histology for a longer term exposure. This is the first histological work using PCAs of known carbon chain length and chlorine content and the first effort to examine the histopathology of fish exposed to PCAs. PCAs, also known as chlorinated paraffins, are complex industrial products for which there is a lack of toxicological data on individual congeners. With the exception of trout exposed to C14H24.9Cl5.1, Which had much lower exposure concentrations, many of the trout exposed to the PCAs (whole fish concentrations 0.22-5.5 mug g(-1)) showed a diminished or no startle response, loss of equilibrium, and developed a dark coloration. These responses are indicative of a narcotic toxicological mode-of-action. Histopathological lesions were observed in the livers of trout from each exposure group, However, the most severe histopathologies were observed in the livers of fish. exposed to C10H15.3Cl6.7 and C11H18.4Cl5.6 (whole fish concentrations 0.92 and 5.5 mug g(-1), respectively), in Which extensive fibrous lesions were present that were not observed in any other exposure group. Other alterations observed in all treatment groups included hepatocyte necrosis, sites of inflammation, and glycogen/lipid depletion. The relative sizes of hepatocytes of PCA exposed trout were smaller than control trout, although only a few of the observed differences were statistically significant. No lesions were present in the thyroid, although trout exposed to C10H15.5Cl6.5 (whole fish concentration 0.84 mug g(-1)) had slightly more active thyroids, as indicated by an increased mean thyroid epithelium cell height relative to controls. It would appear that PCA toxicity is inversely related to carbon chain length, as has been observed in similar studies using mammals. The concentrations in the fish from this experiment were at levels that have been reported in invertebrates and fish from contaminated sites in the Great Lakes. However, the exposure concentrations were likely much greater in these experiments compared with the environment and require further study. (C) 2000 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:81 / 99
页数:19
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