Highlights
- •Examination of acute and long-term effect of DHA on free oxylipin levels in plasma.
- •Up to 600% increase of DHA-oxylipins (HDHAs, EpDPEs, DiHDPEs).
- •Changes in the entire oxylipin profile suggest a cross-linked PUFA metabolism.
- •Slight increase in several EPA-derived hydroxy-FAs and dihydroxy-FAs.
- •Trend to a slight decline in arachidonic acid-derived oxylipin levels.
Abstract
Introduction
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.
Material and methods
The short and long term (1, 3, 6, and 12 week) effect of 1076 mg/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.
Results
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.
Conclusion
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.
Keywords
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Article info
Publication history
Published online: June 14, 2017
Accepted:
June 13,
2017
Received in revised form:
June 12,
2017
Received:
May 5,
2017
Identification
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