Protectin D1 [neuroprotectin D1 (), PD1] has been proposed to play a key role in the resolution of inflammation. Aside from its ω-monohydroxylated metabolite, little has been reported on its metabolic fate. Upon incubation in HepG2 cells, liquid chromatography-tandem mass spectrometry (LC-MS/MS) revealed the formation of two main metabolites, identified as and by comparison with standards obtained through demanding total chemical syntheses. These data represent the first evidence of β-oxidation occurring in specialized proresolving mediators and show that the biotransformation of by human hepatoma cells is extremely rapid and faster than that of leukotriene (). Unlike , the main metabolic process occurs from the polar head chain of . It may limit systemic circulation and prevent its urinary excretion, making difficult its detection and quantitation in vivo. Interestingly, , but not , maintained the bioactivity of the parent , inhibiting neutrophil chemotaxis in vitro and neutrophil tissue infiltration in vivo.
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