Effect of dietary alpha-tocopherol + ascorbic acid, selenium, and iron on oxidative stress in sub-yearling Chinook salmon (Oncorhynchus tshawytscha Walbaum).
A three-variable central composite design coupled with surface-response analysis was used to examine the effects of dietary alpha-tocopherol + ascorbic acid (TOCAA), selenium (Se), and iron (Fe) on indices of oxidative stress in juvenile spring Chinook salmon. Each dietary factor was tested at five levels for a total of fifteen dietary combinations (diets). Oxidative damage in liver and kidney (lipid peroxidation, protein carbonyls) and erythrocytes (erythrocyte resistance to peroxidative lysis, ERPL) was determined after feeding experimental diets for 16 (early December) and 28 (early March) weeks. Only TOCAA influenced oxidative stress in this study, with most measures of oxidative damage decreasing (liver lipid peroxidation in December and March; ERPL in December; liver protein carbonyl in March) with increasing levels of TOCAA. We also observed a TOCAA-stimulated increase in susceptibility of erythrocytes to peroxidative lysis in March at the highest levels of TOCAA. The data suggest that under most circumstances a progressive decrease in oxidative stress occurs as dietary TOCAA increases, but higher TOCAA concentrations can stimulate oxidative damage in some situations. Higher levels of TOCAA in the diet were required in March than in December to achieve comparable levels of protection against oxidative damage, which may have been due to physiological changes associated with the parr-smolt transformation. Erythrocytes appeared to be more sensitive to variation in dietary levels of TOCAA than liver and kidney tissues. Using the March ERPL assay results as a baseline, a TOCAA level of approximately 350-600 mg/kg diet would provide adequate protection against lipid peroxidation under most circumstances in juvenile Chinook salmon.
Welker
T L
TL
United States Department of Agriculture, Agricultural Research Service, Aquatic Animal Health Research Laboratory, 990 Wire Road, Auburn, AL, USA. twelker@ars.usda.gov
Congleton
J L
JL
D000821:Animal Feed; D000824:Animal Nutritional Physiological Phenomena / Q000502:physiology*; D000818:Animals; D000975:Antioxidants / Q000008:administration & dosage / Q000494:pharmacology*; D017756:Aquaculture; D001205:Ascorbic Acid / Q000008:administration & dosage / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004338:Drug Combinations; D004357:Drug Synergism; D004912:Erythrocytes / Q000378:metabolism; D007501:Iron / Q000008:administration & dosage / Q000494:pharmacology; D007668:Kidney / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects*; D008099:Liver / Q000378:metabolism; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000187:drug effects*; D011897:Random Allocation; D012474:Salmon / Q000378:metabolism / Q000502:physiology*; D012643:Selenium / Q000008:administration & dosage / Q000494:pharmacology; D024502:alpha-Tocopherol / Q000008:administration & dosage / Q000494:pharmacology
D000975:Antioxidants; D004338:Drug Combinations; D007501:Iron; D024502:alpha-Tocopherol; D012643:Selenium; D001205:Ascorbic Acid