Farag Aïda M, May Thomas, Marty Gary D, Easton Michael, Harper David D, Little Edward E, Cleveland Laverne
United States Geological Survey, Columbia Environmental Research Center, Jackson Field Research Station, WY 83001, USA.
Aquat Toxicol. 2006 Mar 10;76(3-4):246-57. doi: 10.1016/j.aquatox.2005.09.011. Epub 2005 Dec 5.
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 microgl(-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 microg Crl(-1) for 105 days, neither growth nor survival of parr was affected. On day 105, concentrations were increased from 24 to 120 microg Crl(-1) and from 54 to 266 microg Crl(-1) until the end of the experiment on day 134. Weight of parr was decreased in the 24/120 microg Crl(-1) treatment, and survival was decreased in the 54/266 microg Crl(-1) treatment. Fish health was significantly impaired in both the 24/120 and 54/266 microg Crl(-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 > or =120 microg Crl(-1), nuclear DNA damage followed exposures to 24 microg Crl(-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 > or =120 microg Crl(-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.
本研究旨在确定暴露于铬的奇努克鲑（Oncorhynchus tshawytscha）的鱼类健康损害情况。将幼年奇努克鲑暴露于美国西北部哥伦比亚河鲑鱼产卵区底部沉积物孔隙水和井水记录的水相铬浓度（0 - 266微克/升）中。奇努克鲑幼鱼暴露于24微克/升和54微克/升的铬105天后，幼鱼的生长和存活均未受到影响。在第105天，浓度分别从24微克/升增加到120微克/升以及从54微克/升增加到266微克/升，直至第134天实验结束。在24/120微克/升铬处理组中幼鱼体重下降，在54/266微克/升铬处理组中存活率下降。在24/120微克/升和54/266微克/升铬处理组中鱼类健康均受到显著损害。在通过水柱暴露于铬的过程中，肾脏是靶器官。暴露于最高铬浓度的鱼类肾脏出现肉眼可见和微观的病变（如肾小管内衬细胞坏死），脂质过氧化产物升高。这些变化与肾脏中铬浓度升高、生长和存活降低有关。此外，血液中DNA的变化与肾脏和脾脏的病理变化有关。这些变化表明铬积累并进入脂质过氧化途径，在此发生脂肪酸损伤和DNA损伤（表现为染色体变化），从而导致细胞死亡和组织损伤。虽然大多数生理功能障碍发生在幼鱼暴露于浓度≥120微克/升铬之后，但核DNA损伤在暴露于24微克/升铬（测试的最小浓度）后就出现了。本研究中测量到的异常情况尤为重要，因为它们与浓度≥120微克/升铬时生长受损和存活率降低有关。因此，这些变化可用于调查高铬浓度天然水域中常驻鱼类的健康状况，并深入了解铬毒性的机制。
