Examination of the behavior and liver and thyroid histology of juvenile rainbow trout (Oncorhynchus mykiss) exposed to high dietary concentrations ofC-10-, C-11-, C-12- and C-14-polychlorinated n-alkanes

Citation
Hm. Cooley et al., Examination of the behavior and liver and thyroid histology of juvenile rainbow trout (Oncorhynchus mykiss) exposed to high dietary concentrations ofC-10-, C-11-, C-12- and C-14-polychlorinated n-alkanes, AQUAT TOX, 54(1-2), 2001, pp. 81-99
Citations number
53
Categorie Soggetti
Aquatic Sciences
Journal title
AQUATIC TOXICOLOGY
ISSN journal
0166445X → ACNP
Volume
54
Issue
1-2
Year of publication
2001
Pages
81 - 99
Database
ISI
SICI code
0166-445X(200109)54:1-2<81:EOTBAL>2.0.ZU;2-1
Abstract
Juvenile rainbow trout (Oncorhynchus mykiss) Were exposed to high dietary c oncentrations 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 C14 H23.3Cl6.7) for 21 to assess their effects on behavior and liver and thyroi d 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 lengt h and chlorine content and the first effort to examine the histopathology o f fish exposed to PCAs. PCAs, also known as chlorinated paraffins, are comp lex 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 diminishe d or no startle response, loss of equilibrium, and developed a dark colorat ion. These responses are indicative of a narcotic toxicological mode-of-act ion. Histopathological lesions were observed in the livers of trout from ea ch exposure group, However, the most severe histopathologies were observed in the livers of fish. exposed to C10H15.3Cl6.7 and C11H18.4Cl5.6 (whole fi sh 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 hepatocy te necrosis, sites of inflammation, and glycogen/lipid depletion. The relat ive sizes of hepatocytes of PCA exposed trout were smaller than control tro ut, although only a few of the observed differences were statistically sign ificant. 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 a ctive thyroids, as indicated by an increased mean thyroid epithelium cell h eight relative to controls. It would appear that PCA toxicity is inversely related to carbon chain length, as has been observed in similar studies usi ng mammals. The concentrations in the fish from this experiment were at lev els that have been reported in invertebrates and fish from contaminated sit es in the Great Lakes. However, the exposure concentrations were likely muc h greater in these experiments compared with the environment and require fu rther study. (C) 2000 Elsevier Science B.V. All rights reserved.