期刊
JOURNAL OF NUTRITION
卷 141, 期 12, 页码 2113-2118出版社
OXFORD UNIV PRESS
DOI: 10.3945/jn.111.144279
关键词
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资金
- National Institute of Environmental Health Sciences [P30 ES000210]
- National Institute of Child Health and Human Development [HD062109]
- NIH Diabetes and Digestive and Kidney Diseases [43220]
- United States Department of Agriculture/National Institute of Food and Agriculture [2009-65200-05846]
- NIFA [581537, 2009-65200-05846] Funding Source: Federal RePORTER
alpha-Tocopherol is a required, lipid-soluble antioxidant that protects PUFA. We hypothesized that alpha-tocopherol deficiency in zebrafish compromises PUFA status. Zebrafish were fed for 1 y either an alpha-tocopherol-sufficient (E+; 500 mg alpha-tocopherol/kg) or -deficient (E-; 1.1 mg alpha-tocopherol/kg) diet containing alpha-linolenic (ALA) and linoleic (LA) acids but without arachidonic acid (ARA), EPA, or DHA. Vitamin E deficiency in zebrafish decreased by similar to 20% (n-6) (P < 0.05) and (n-3) (P < 0.05) PUFA and increased the (n-6):(n-3) PUFA ratio (P < 0.05). In E- compared to E+ females, long chain-PUFA status was impaired, as assessed by a similar to 60% lower DHA:ALA ratio (P < 0.05) and a similar to 50% lower ARA:LA ratio (P < 0.05). fads2 (P < 0.05) and elovl2 (P < 0.05) mRNA expression was doubled in E- compared to E+ fish. Thus, inadequate vitamin E status led to a depletion of PUFA that may be a result of either or both increased lipid peroxidation and an impaired ability to synthesize sufficient PUFA, especially (n-3) PUFA. J. Nutr. 141: 2113-2118, 2011.
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