Assessing the sensitivity of Atlantic salmon (Salmo salar) to dietary endosulfan exposure using tissue biochemistry and histology.
The incorporation of plant-based ingredients, and the possible carry-over of pesticides such as endosulfan, in fish feeds may present new toxicological challenges to aquacultural species. Biological responses of Atlantic salmon (Salmo salar) to a 35-day dietary endosulfan exposure at levels ranging from 4 to 710 microgkg(-1) were assessed using tissue histology and biochemistry. Liver 7-ethoxyresorufin-O-deacetylase (EROD) activity was significantly elevated in the highest exposure group (710 microgkg(-1)) by day 35. Other hepatic indicators of stress impacts and responses (glutathione-S-transferase and glutathione peroxidase activities and hepatic alpha-tocopherol content) remained unchanged. Branchial Na(+), K(+)-ATPase activity was significantly reduced at day 14 in the highest exposure group, but returned to control levels by day 35. Conversely, intestinal Na(+), K(+)-ATPase activity was significantly inhibited at day 35, but again only at the highest exposure level. In contrast to the biochemical results, hepatic and intestinal histology revealed effects of exposure even at the lowest dose tested (4 microgkg(-1)). In the posterior intestine, pathology was characterised by vacuolation and fusion of villi, and in the most severe cases, loss of epithelial integrity in villi tips. In the liver the primary effects were glycogen depletion and lipidosis. These changes were typical of a generalised stress response. While histology endpoints may prove to be the most sensitive indicators of dietary endosulfan exposure, the organismal relevance of these structural changes must be considered in the absence of effects in other biomarkers at dietary levels less than 710 microgkg(-1).
Glover
Chris N
CN
National Institute of Nutrition and Seafood Research (NIFES), Bergen, Norway.
Petri
Dietrich
D
National Institute of Nutrition and Seafood Research (NIFES), Bergen, Norway.
Tollefsen
Knut-Erik
KE
Norwegian Institute for Water Research (NIVA), Oslo, Norway.
Jørum
Nanne
N
Skretting ARC, Stavanger, Norway.
Handy
Richard D
RD
School of Biological Sciences, University of Plymouth, Plymouth, United Kingdom.
Berntssen
Marc H G
MHG
National Institute of Nutrition and Seafood Research (NIFES), Bergen, Norway. Electronic address: marc.berntssen@nifes.no.
D000821:Animal Feed / Q000009:adverse effects*; D000818:Animals; D017756:Aquaculture; D019363:Cytochrome P-450 CYP1A1 / Q000378:metabolism; D004726:Endosulfan / Q000493:pharmacokinetics / Q000633:toxicity*; D005979:Glutathione Peroxidase / Q000378:metabolism; D005982:Glutathione Transferase / Q000378:metabolism; D006651:Histocytochemistry; D007306:Insecticides / Q000633:toxicity*; D007413:Intestinal Mucosa / Q000378:metabolism; D007422:Intestines / Q000187:drug effects / Q000201:enzymology / Q000473:pathology; D008099:Liver / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism / Q000473:pathology; D020317:Salmo salar / Q000378:metabolism*; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D014874:Water Pollutants, Chemical / Q000493:pharmacokinetics / Q000633:toxicity*; D024502:alpha-Tocopherol / Q000378:metabolism
D007306:Insecticides; D014874:Water Pollutants, Chemical; D005979:Glutathione Peroxidase; D019363:Cytochrome P-450 CYP1A1; D005982:Glutathione Transferase; D000254:Sodium-Potassium-Exchanging ATPase; D024502:alpha-Tocopherol; D004726:Endosulfan