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Zebrafish as a model to determine the mechanisms of vitamin E function
Author(s) -
Miller Galen W,
Labut Edwin M,
Lebold Katie,
Floeter Abby,
Tanguay Robert L,
Traber Maret G
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.534.1
Subject(s) - zebrafish , fish <actinopterygii> , fetus , embryo , human fertilization , resorption , biology , vitamin , vitamin e , andrology , medicine , embryogenesis , animal model , endocrinology , physiology , zoology , pregnancy , anatomy , biochemistry , microbiology and biotechnology , genetics , fishery , antioxidant , gene
Vitamin E (alpha‐tocopherol, AT) is required to prevent fetal resorption in rodents. To study its role in fetal development, a non‐placental model is required. Therefore, we have developed an AT‐deficient zebrafish model by feeding a defined diet (with or without AT) that we created. Zebrafish (age: 1 m) were fed the deficient (E−), sufficient (E+), or Lab diet up to 1 y. All groups showed similar growth and normal development. When compared to E+, the E− fish had lower (p<0.05) AT levels within 3 w; by 112 d the E− fish (3±1 nmol/g) contained 100 fold less AT than the E+ fish (375±100, p<0.001). The rate of depletion was 0.029 ± 0.006 pools/d. At age ~4 m, E‐depleted adults were spawned and produced viable embryos with similar AT concentrations to those of their parents. The E− embryos exhibited a higher mortality at 24 h post fertilization (hpf) and a higher combination of malformations and mortality at 120 hpf than the control diets. This study documents for the first time that vitamin E is essential for normal embryonic development. It also shows that the zebrafish is an exceptional model to define the molecular functions of vitamin E. Grant Funding Source : NIH #HD062109 and #ES00210