Schuchardt Jan Philipp, Ostermann Annika I, Stork Lisa, Fritzsch Sabrina, Kohrs Heike, Greupner Theresa, Hahn Andreas, Schebb Nils Helge
Institute of Food Science and Human Nutrition, Faculty of Natural Sciences, Leibniz University Hannover, Germany.
Institute for Food Toxicology and Analytical Chemistry, University of Veterinary Medicine Hannover, Germany.
Prostaglandins Leukot Essent Fatty Acids. 2017 Jun;121:76-87. doi: 10.1016/j.plefa.2017.06.007. Epub 2017 Jun 15.
EPA and DHA cause different physiological effects, which are in many cases mediated via their oxidative metabolites (oxylipins). However, metabolism studies investigating the effect of either EPA or DHA on comprehensive oxylipin patterns are lacking.
The short and long term (1, 3, 6, and 12 week) effect of 1076mg/d DHA (free of EPA) on free (unesterified) oxylipin concentrations in plasma and lipopolysacharid (LPS) stimulated blood of 12 healthy men (mean age 25.1 ± 1.5 years) was investigated.
After DHA supplementation, plasma levels of all DHA-oxylipins (HDHAs, EpDPEs, DiHDPEs) significantly increased (up to 600%) in a time-dependent fashion. Oxylipins of EPA and arachidonic acid (AA) were also affected. Whereas a slight increase in several EPA-derived hydroxy-FAs (including the RvE1 precursor 18-HEPE) and dihydroxy-FAs was observed after DHA supplementation, a trend to a slight decline in AA-derived oxylipin levels was found. In LPS stimulated blood, it is shown that DHA supplementation significantly reduces the ability of immune cells to form AA-derived COX (TXB2 and PGB2) and 12-LOX (12-HETE) eicosanoids. While no increase in EPA COX metabolites was found, n-3 PUFA 12-LOX metabolites of EPA (12-HEPE) and DHA (14-HDHA) were highly induced.
We demonstrated that DHA supplementation causes a time-dependent shift in the entire oxylipin profile suggesting a cross-linked metabolism of PUFAs and subsequent formation of oxygenated lipid mediators.
二十碳五烯酸（EPA）和二十二碳六烯酸（DHA）会产生不同的生理效应，在许多情况下，这些效应是通过它们的氧化代谢产物（氧化脂质）介导的。然而，目前缺乏关于EPA或DHA对综合氧化脂质模式影响的代谢研究。
研究了1076mg/d的DHA（不含EPA）对12名健康男性（平均年龄25.1±1.5岁）血浆中游离（未酯化）氧化脂质浓度以及脂多糖（LPS）刺激血液的短期和长期（1、3、6及12周）影响。
补充DHA后，所有DHA氧化脂质（HDHA、EpDPE、DiHDPE）的血浆水平均呈时间依赖性显著升高（高达600%）。EPA和花生四烯酸（AA）的氧化脂质也受到影响。补充DHA后，观察到几种EPA衍生的羟基脂肪酸（包括RvE1前体18-HEPE）和二羟基脂肪酸略有增加，而AA衍生的氧化脂质水平有轻微下降趋势。在LPS刺激的血液中，结果表明补充DHA可显著降低免疫细胞形成AA衍生的环氧化酶（TXB2和PGB2）和12-脂氧合酶（12-HETE）类花生酸的能力。虽然未发现EPA环氧化酶代谢产物增加，但EPA（12-HEPE）和DHA（14-HDHA）的n-3多不饱和脂肪酸12-脂氧合酶代谢产物被高度诱导。
我们证明，补充DHA会导致整个氧化脂质谱随时间发生变化，这表明多不饱和脂肪酸存在交联代谢以及随后氧化脂质介质的形成。
