Abstract

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 a-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 peroxidtion and an impaired ability to synthesize sufficient PUFA, especially (n-3) PUFA.

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