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      Oleic acid increases mitochondrial reactive oxygen species production and decreases endothelial nitric oxide synthase activity in cultured endothelial cells.

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          Abstract

          Elevated plasma levels of free fatty acids (FFA) are associated with increased cardiovascular risk. This may be related to FFA-induced elevation of oxidative stress in endothelial cells. We hypothesized that, in addition to mitochondrial production of reactive oxygen species, endothelial nitric oxide synthase (eNOS)-mediated reactive oxygen species production contributes to oleic acid (OA)-induced oxidative stress in endothelial cells, due to eNOS uncoupling. We measured reactive oxygen species production and eNOS activity in cultured endothelial cells (bEnd.3) in the presence of OA bound to bovine serum albumin, using the CM-H2DCFDA assay and the L-arginine/citrulline conversion assay, respectively. OA induced a concentration-dependent increase in reactive oxygen species production, which was inhibited by the mitochondrial complex II inhibitor thenoyltrifluoroacetone (TTFA). OA had little effect on eNOS activity when stimulated by a calcium-ionophore, but decreased both basal and insulin-induced eNOS activity, which was restored by TTFA. Pretreatment of bEnd.3 cells with tetrahydrobiopterin (BH4) prevented OA-induced reactive oxygen species production and restored inhibition of eNOS activity by OA. Elevation of OA levels leads to both impairment in receptor-mediated stimulation of eNOS and to production of mitochondrial-derived reactive oxygen species and hence endothelial dysfunction.

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          Author and article information

          Journal
          Eur. J. Pharmacol.
          European journal of pharmacology
          1879-0712
          0014-2999
          Mar 15 2015
          : 751
          Affiliations
          [1 ] Department of Nephrology and Hypertension, University Medical Center Utrecht, Utrecht, The Netherlands.
          [2 ] Department of Medicine, Division of Nephrology and Immunology, University of Alberta Hospital, Edmonton, Canada; Department of Physiology, University of Alberta, Edmonton, Canada.
          [3 ] Department of Nephrology and Hypertension, University Medical Center Utrecht, Utrecht, The Netherlands. Electronic address: J.A.Joles@umcutrecht.nl.
          Article
          S0014-2999(15)00025-4
          10.1016/j.ejphar.2015.01.005
          25595727
          5762f28c-6803-4bbe-a64f-4f33ce820a4b
          Copyright © 2015 Elsevier B.V. All rights reserved.
          History

          Endothelium,Fatty acids,Nitric oxide synthase,Oleic acid,Reactive oxygen species

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