TY - JOUR U1 - Wissenschaftlicher Artikel A1 - Gollasch, Benjamin A1 - Wu, Guanlin A1 - Liu, Tong A1 - Dogan, Inci A1 - Rothe, Michael A1 - Gollasch, Maik A1 - Luft, Friedrich C. T1 - Hemodialysis and erythrocyte epoxy fatty acids JF - Physiological Reports N2 - Abstract Fatty acid products derived from cytochromes P450 (CYP) monooxygenase and lipoxygenase (LOX)/CYP ω/(ω‐1)‐hydroxylase pathways are a superclass of lipid mediators with potent bioactivities. Whether or not the chronic kidney disease (CKD) and hemodialysis treatments performed on end‐stage renal disease (ESRD) patients affect RBC epoxy fatty acids profiles remains unknown. Measuring the products solely in plasma is suboptimal. Since such determinations invariably ignore red blood cells (RBCs) that make up 3 kg of the circulating blood. RBCs are potential reservoirs for epoxy fatty acids that regulate cardiovascular function. We studied 15 healthy persons and 15 ESRD patients undergoing regular hemodialysis treatments. We measured epoxides derived from CYP monooxygenase and metabolites derived from LOX/CYP ω/(ω‐1)‐hydroxylase pathways in RBCs by LC–MS/MS tandem mass spectrometry. Our data demonstrate that various CYP epoxides and LOX/CYP ω/(ω‐1)‐hydroxylase products are increased in RBCs of ESRD patients, compared to control subjects, including dihydroxyeicosatrienoic acids (DHETs), epoxyeicosatetraenoic acids (EEQs), dihydroxydocosapentaenoic acids (DiHDPAs), and hydroxyeicosatetraenoic acids (HETEs). Hemodialysis treatment did not affect the majority of those metabolites. Nevertheless, we detected more pronounced changes in free metabolite levels in RBCs after dialysis, as compared with the total RBC compartment. These findings indicate that free RBC eicosanoids should be considered more dynamic or vulnerable in CKD. KW - - KW - chronic kidney disease (CKD) KW - dialysis KW - erythrocytes KW - fatty acids KW - lipidomics Y1 - 2020 UN - https://nbn-resolving.org/urn:nbn:de:gbv:9-opus-41422 U6 - https://doi.org/10.14814/phy2.14601 DO - https://doi.org/10.14814/phy2.14601 VL - 8 IS - 20 ER -