Vitamin E Deficiency Decreases Long-Chain PUFA in Zebrafish (Danio rerio)
Author(s) -
Katie M. Lebold,
Donald Β. Jump,
Galen W. Miller,
Charlotte L. Wright,
Edwin M. Labut,
Carrie L. Barton,
Robert L. Tanguay,
Maret G. Traber
Publication year - 2011
Publication title -
journal of nutrition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.463
H-Index - 265
eISSN - 1541-6100
pISSN - 0022-3166
DOI - 10.3945/jn.111.144279
Subject(s) - polyunsaturated fatty acid , zebrafish , vitamin e , linoleic acid , arachidonic acid , tocopherol , vitamin e deficiency , endocrinology , medicine , fads2 , chemistry , vitamin , antioxidant , long chain , biology , biochemistry , docosahexaenoic acid , fatty acid , enzyme , gene , polymer science
α-Tocopherol is a required, lipid-soluble antioxidant that protects PUFA. We hypothesized that α-tocopherol deficiency in zebrafish compromises PUFA status. Zebrafish were fed for 1 y either an α-tocopherol-sufficient (E+; 500 mg α-tocopherol/kg) or -deficient (E-; 1.1 mg α-tocopherol/kg) diet containing α-linolenic (ALA) and linoleic (LA) acids but without arachidonic acid (ARA), EPA, or DHA. Vitamin E deficiency in zebrafish decreased by ~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 ~60% lower DHA:ALA ratio (P < 0.05) and a ~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.
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