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2 results on '"N-linoleoyl-ethanolamine"'

1. Biosynthesis of the Novel Endogenous 15-Lipoxygenase Metabolites

Author

Anne-Sophie, Archambault, Francesco, Tinto, Élizabeth, Dumais, Volatiana, Rakotoarivelo, Magdalena, Kostrzewa, Pier-Luc, Plante, Cyril, Martin, Mélissa, Simard, Cristoforo, Silvestri, Roxane, Pouliot, Michel, Laviolette, Louis-Philippe, Boulet, Rosa Maria, Vitale, Alessia, Ligresti, Vincenzo, Di Marzo, and Nicolas, Flamand

Subjects
linoleic acid, Neutrophils, Peroxisome Proliferator-Activated Receptors, TRPV Cation Channels, endocannabinoid, 13-HODE, Article, Substrate Specificity, Eosinophils, Molecular Docking Simulation, Kinetics, Mice, N-linoleoyl-ethanolamine, Linoleic Acids, eicosanoid, Animals, Arachidonate 15-Lipoxygenase, Humans, anandamide, lipids (amino acids, peptides, and proteins), linoleoyl-glycerol, Receptors, Cannabinoid, 2-arachidonoyl-glycerol, Protein Binding
Abstract

The endocannabinoids 2-arachidonoyl-glycerol and N-arachidonoyl-ethanolamine are lipids regulating many physiological processes, notably inflammation. Endocannabinoid hydrolysis inhibitors are now being investigated as potential anti-inflammatory agents. In addition to 2-arachidonoyl-glycerol and N-arachidonoyl-ethanolamine, the endocannabinoidome also includes other monoacylglycerols and N-acyl-ethanolamines such as 1-linoleoyl-glycerol (1-LG) and N-linoleoyl-ethanolamine (LEA). By increasing monoacylglycerols and/or N-acyl-ethanolamine levels, endocannabinoid hydrolysis inhibitors will likely increase the levels of their metabolites. Herein, we investigated whether 1-LG and LEA were substrates for the 15-lipoxygenase pathway, given that both possess a 1Z,4Z-pentadiene motif, near their omega end. We thus assessed how human eosinophils and neutrophils biosynthesized the 15-lipoxygenase metabolites of 1-LG and LEA. Linoleic acid (LA), a well-documented substrate of 15-lipoxygenases, was used as positive control. N-13-hydroxy-octodecadienoyl-ethanolamine (13-HODE-EA) and 13-hydroxy-octodecadienoyl-glycerol (13-HODE-G), the 15-lipoxygenase metabolites of LEA and 1-LG, were synthesized using Novozym 435 and soybean lipoxygenase. Eosinophils, which express the 15-lipoxygenase-1, metabolized LA, 1-LG, and LEA into their 13-hydroxy derivatives. This was almost complete after five minutes. Substrate preference of eosinophils was LA > LEA > 1-LG in presence of 13-HODE-G hydrolysis inhibition with methyl-arachidonoyl-fluorophosphonate. Human neutrophils also metabolized LA, 1-LG, and LEA into their 13-hydroxy derivatives. This was maximal after 15–30 s. Substrate preference was LA ≫ 1-LG > LEA. Importantly, 13-HODE-G was found in humans and mouse tissue samples. In conclusion, our data show that human eosinophils and neutrophils metabolize 1-LG and LEA into the novel endogenous 15-lipoxygenase metabolites 13-HODE-G and 13-HODE-EA. The full biological importance of 13-HODE-G and 13-HODE-EA remains to be explored.

Published
2021

2. Biosynthesis of the Novel Endogenous 15-Lipoxygenase Metabolites N -13-Hydroxy-octodecadienoyl-ethanolamine and 13-Hydroxy-octodecadienoyl-glycerol by Human Neutrophils and Eosinophils.

Author

Archambault AS, Tinto F, Dumais É, Rakotoarivelo V, Kostrzewa M, Plante PL, Martin C, Simard M, Silvestri C, Pouliot R, Laviolette M, Boulet LP, Vitale RM, Ligresti A, Di Marzo V, and Flamand N

Subjects
Animals, Humans, Kinetics, Mice, Molecular Docking Simulation, Peroxisome Proliferator-Activated Receptors metabolism, Protein Binding, Receptors, Cannabinoid metabolism, Substrate Specificity, TRPV Cation Channels metabolism, Arachidonate 15-Lipoxygenase metabolism, Eosinophils enzymology, Linoleic Acids metabolism, Neutrophils enzymology
Abstract

The endocannabinoids 2-arachidonoyl-glycerol and N -arachidonoyl-ethanolamine are lipids regulating many physiological processes, notably inflammation. Endocannabinoid hydrolysis inhibitors are now being investigated as potential anti-inflammatory agents. In addition to 2-arachidonoyl-glycerol and N -arachidonoyl-ethanolamine, the endocannabinoidome also includes other monoacylglycerols and N -acyl-ethanolamines such as 1-linoleoyl-glycerol (1-LG) and N -linoleoyl-ethanolamine (LEA). By increasing monoacylglycerols and/or N -acyl-ethanolamine levels, endocannabinoid hydrolysis inhibitors will likely increase the levels of their metabolites. Herein, we investigated whether 1-LG and LEA were substrates for the 15-lipoxygenase pathway, given that both possess a 1 Z ,4 Z -pentadiene motif, near their omega end. We thus assessed how human eosinophils and neutrophils biosynthesized the 15-lipoxygenase metabolites of 1-LG and LEA. Linoleic acid (LA), a well-documented substrate of 15-lipoxygenases, was used as positive control. N -13-hydroxy-octodecadienoyl-ethanolamine (13-HODE-EA) and 13-hydroxy-octodecadienoyl-glycerol (13-HODE-G) , the 15-lipoxygenase metabolites of LEA and 1-LG, were synthesized using Novozym 435 and soybean lipoxygenase. Eosinophils, which express the 15-lipoxygenase-1, metabolized LA, 1-LG, and LEA into their 13-hydroxy derivatives. This was almost complete after five minutes. Substrate preference of eosinophils was LA > LEA > 1-LG in presence of 13-HODE-G hydrolysis inhibition with methyl-arachidonoyl-fluorophosphonate. Human neutrophils also metabolized LA, 1-LG, and LEA into their 13-hydroxy derivatives. This was maximal after 15-30 s. Substrate preference was LA ≫ 1-LG > LEA. Importantly, 13-HODE-G was found in humans and mouse tissue samples. In conclusion, our data show that human eosinophils and neutrophils metabolize 1-LG and LEA into the novel endogenous 15-lipoxygenase metabolites 13-HODE-G and 13-HODE-EA. The full biological importance of 13-HODE-G and 13-HODE-EA remains to be explored.

Published
2021
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