Submitted to: Aquaculture Research
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/28/2004
Publication Date: 7/1/2004
Citation: Welker, T.L., Congleton, J. 2004. Effect of a low-water stressor on oxidative stress in sub-yearling chinook salmon (Oncorhynchus tshawytscha). Aquaculture Research, 35: 881-887.
Interpretive Summary: Oxidative stress, produced as a consequence of normal cellular metabolism, can cause damage in biological systems and has been implicated in the pathogenesis of many diseases in humans and also in fish. Recent evidence indicates that the physiological response to stress leads to oxidative stress in mammals, and although there is ample evidence to support a relationship between oxidative stress and the stress response in mammals, the relationship has received little examination in fish. Stress can adversely affect the health of fish under intensive culture conditions. Therefore, this study was conducted to examine the effect of a low-water stressor on oxidative stress. The results show that the application of a low-water stressor causes an increase in oxidative stress-mediated damage to kidney and brain but not liver after 48 h in juvenile chinook salmon. These findings have implications for stress management in fish hatcheries. Stress associated with intensive fish culture (e.g. handling, crowding, temperature, and water quality) may increase the production of free radicals, depleting fish of vital antioxidant vitamins and nutrients and lead to tissue damage. Diets containing enhanced levels of antioxidants may be beneficial for fish that are frequently exposed to stress.
Technical Abstract: Juvenile chinook salmon Oncorhynchus tshawytscha were subjected to a low-water stressor to determine the relationship between the general stress response and oxidative stress. Lipid peroxidation (LPO) levels were measured in kidney, liver, and brain samples taken at the beginning of the experiment (0-h unstressed controls) and at 6, 24, and 48 h after application of a continuous low-water stressor. Tissue samples were also taken at 48 h from fish that had not been exposed to the stressor (48-h unstressed controls). Exposure to the low-water stressor affected LPO in kidney (P = 0.004, R2 = 0.58) and brain (P = 0.10, R2 = 0.34) tissues. In kidney, LPO decreased (P = 0.06, g = 1.4) 6 h after imposition of the stressor; similar but less pronounced decreases also occurred in liver (P = 1.0, g = 0.32) and brain (P = 1.0, g = 0.44). At 48 h, LPO increased (in comparison with 6-h stressed tissues) in kidney (P = 0.09, g = 2.3) and brain (P = 0.025, g = 1.4). A similar but smaller increase was observed in liver tissue (P = 0.80; g = 0.77). In comparison with 48-h unstressed controls, LPO levels were higher in the kidney (P = 0.001, g = 2.8) and brain (P = 0.016, g = 1.6) of stressed fish. This is the first demonstration of a relationship between the general stress response and oxidative stress in fish.