Novel function of vitamin E in regulation of zebrafish (Danio rerio) brain lysophospholipids discovered using lipidomics

Novel function of vitamin E in regulation of zebrafish (Danio rerio) brain lysophospholipids discovered using lipidomics
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DOI:
10.1194/jlr.m058941
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发表时间:
2015-06-01
影响因子:
6.5
通讯作者:
Traber, Maret G.
Traber, Maret G.
中科院分区:
生物学2区
文献类型:
--
作者:
Choi, Jaewoo;Leonard, Scott W.;Traber, Maret G.

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我们假设,从维生素E缺乏(E-)斑马鱼(Danio rerio)的大脑将经历增加的脂质过氧化,因为它们含有高度多不饱和脂肪酸,从而可以确定易感脂质。研究了喂食9个月不含(E-)或含(E+)添加维生素E(500 mg RRR-alpha-生育酚乙酸酯/千克饲料)的规定饲料的斑马鱼脑。使用非靶向方法,1-十六酰基-2-二十二碳六烯酰基-sn-甘油-3-磷酸胆碱[DHA-PC 38:6,PC 16:0/22:6]是组间显示最显著和最大倍数差异的脂质。与E+脑(6.5 +/- 0.9 mg/g,平均值+/- SEM,n = 10/组,P = 0.04)相比,E-脑(4.3 +/- 0.6 mg/g)中的DHA-PC浓度约低1/3。使用脂质组学,脑提取物中的155种脂质被鉴定。只有四种磷脂(PL)在组间不同(P < 0.05);它们在E-脑中较低,含有DHA,DHA-PC 38:6的丰度最高。此外,羟基-DHA-PC 38:6在E-脑中增加(P = 0.0341),支持DHA过氧化的假设。更引人注目的是E-脑中19种不同溶血磷脂(lysoPL)中近60%的消耗(合并P = 0.0003),这对膜PL重塑至关重要。因此,E-脑含有较少的DHA-PL,较多的羟基-DHA-PC和较少的lysoPL,表明脂质过氧化消耗膜DHA-PC和稳态机制来修复导致lysoPL消耗的损伤
We hypothesized that brains from vitamin E-deficient (E-) zebrafish (Danio rerio) would undergo increased lipid peroxidation because they contain highly polyunsaturated fatty acids, thus susceptible lipids could be identified. Brains from zebrafish fed for 9 months defined diets without (E-) or with (E+) added vitamin E (500 mg RRR-alpha-tocopheryl acetate per kilogram diet) were studied. Using an untargeted approach, 1-hexadecanoyl-2-docosahexaenoyl-sn -glycero-3-phosphocholine [DHA-PC 38: 6, PC 16:0/22:6] was the lipid that showed the most significant and greatest fold-differences between groups. DHA-PC concentrations were approximately 1/3 lower in E- (4.3 +/- 0.6 mg/g) compared with E+ brains (6.5 +/- 0.9 mg/g, mean +/- SEM, n = 10 per group, P = 0.04). Using lipidomics, 155 lipids in brain extracts were identified. Only four phospholipids (PLs) were different (P < 0.05) between groups; they were lower in E-brains and contained DHA with DHA-PC 38: 6 at the highest abundances. Moreover, hydroxy-DHA-PC 38: 6 was increased in E-brains (P = 0.0341) supporting the hypothesis of DHA peroxidation. More striking was the depletion in E-brains of nearly 60% of 19 different lysophospholipids (lysoPLs) (combined P = 0.0003), which are critical for membrane PL remodeling. Thus, E-brains contained fewer DHA-PLs, more hydroxy-DHA-PCs, and fewer lysoPLs, suggesting that lipid peroxidation depletes membrane DHA-PC and homeostatic mechanisms to repair the damage resulting in lysoPL depletion