|The effect of chronic chromium exposure on the health of Chinook salmon (Oncorhynchus tshawytscha)|Farag, A.M.; May, T.; Marty, G.D.; Easton, M.; Harper, D.D.; Little, E.E.; Cleveland, L. (2006). The effect of chronic chromium exposure on the health of Chinook salmon (Oncorhynchus tshawytscha). Aquat. Toxicol. 76(3-4): 246-257. dx.doi.org/10.1016/j.aquatox.2005.09.011
In: Aquatic Toxicology. Elsevier Science: Tokyo; New York; London; Amsterdam. ISSN 0166-445X, more
Chromium; DNA; Histology; Lipids; [WoRMS]; USA, Washington, Columbia R. [Marine Regions]; Marine; Brackish water; Fresh water
|Authors|| || Top |
- Farag, A.M.
- May, T.
- Marty, G.D.
- Easton, M.
- Harper, D.D.
- Little, E.E.
- Cleveland, L.
This study was designed to determine fish health impairment of Chinook salmon (Oncorhynchus tshawytscha) exposed to chromium. Juvenile Chinook salmon were exposed to aqueous chromium concentrations (0–266 μg l−1) that have been documented in porewater from bottom sediments and in well waters near salmon spawning areas in the Columbia River in the northwestern United States. After Chinook salmon parr were exposed to 24 and 54 μg Cr l−1 for 105 days, neither growth nor survival of parr was affected. On day 105, concentrations were increased from 24 to 120 μg Cr l−1 and from 54 to 266 μg Cr l−1 until the end of the experiment on day 134. Weight of parr was decreased in the 24/120 μg Cr l−1 treatment, and survival was decreased in the 54/266 μg Cr l−1 treatment. Fish health was significantly impaired in both the 24/120 and 54/266 μg Cr l−1 treatments. The kidney is the target organ during chromium exposures through the water column. The kidneys of fish exposed to the greatest concentrations of chromium had gross and microscopic lesions (e.g. necrosis of cells lining kidney tububules) and products of lipid peroxidation were elevated. These changes were associated with elevated concentrations of chromium in the kidney, and reduced growth and survival. Also, variations in DNA in the blood were associated with pathological changes in the kidney and spleen. These changes suggest that chromium accumulates and enters the lipid peroxidation pathway where fatty acid damage and DNA damage (expressed as chromosome changes) occur to cause cell death and tissue damage. While most of the physiological malfunctions occurred following parr exposures to concentrations ≥120 μg Cr l−1, nuclear DNA damage followed exposures to 24 μg Cr l−1, which was the smallest concentration tested. The abnormalities measured during this study are particularly important because they are associated with impaired growth and reduced survival at concentrations ≥120 μg Cr l−1. Therefore, these changes can be used to investigate the health of resident fish in natural waters with high chromium concentrations as well as provide insight into the mechanisms of chromium toxicity.