PMC:7335494 / 57269-58166 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7335494","sourcedb":"PMC","sourceid":"7335494","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7335494","text":"Besides decreasing production of PGE2, DHA and EPA are also substrates for the biosynthesis of lipid derivatives, but the EPA-derived mediators as series-3 prostaglandins (PGD3) or series-5 leukotrienes are typically less biologically potent, having a lower ability to interact with relevant eicosanoid receptors (Calder, 2015). For example, EPA-derived leukotriene B5 (LTB5) is almost 100 times less active as a leukocyte chemoattractant than ARA-derived LTB4 (Calder, 2017). However, in some cases, EPA-derived mediators have similar potency with ARA-derived mediators. It appears that EPA-derived PGD3 inhibits the effect of the ARA-derived PGD2, due to a stronger interaction with the DP1 receptor compared to PGD2 (Wada et al., 2007). In other cases, EPA-derived mediators exhibited a similar magnitude of effect (e.g. inhibition of TNF-α production by blood monocytes) (Dooper et al., 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