Treatment with n-3 polyunsaturated fatty acids reverses endothelial dysfunction and oxidative stress in experimental menopause

J Nutr Biochem. 2013 Jan;24(1):371-9. doi: 10.1016/j.jnutbio.2012.07.012. Epub 2012 Nov 14.

Abstract

Menopause is associated with endothelial dysfunction and oxidative stress. In this condition, reduced n-3 polyunsaturated fatty acids (n-3 PUFAs) contribute to cardiovascular disease. We investigated whether treatment with n-3 PUFA reverses endothelial dysfunction and oxidative stress in experimental menopause. Thirty female rats underwent either sham-surgery or bilateral ovariectomy or bilateral ovariectomy+oral n-3 PUFA (0.8 g kg(-1) day(-1) for 2 months). Ovariectomy caused endothelial dysfunction to acetylcholine, which was reversed by superoxide scavenger Tiron. Erythrocyte membrane lipid composition was characterized by reduced n-3 PUFA total content and omega-3 index, and by concomitant increase in n-6:n-3 PUFA ratio. Ovariectomy-related oxidative stress, demonstrated by both enhanced superoxide production and 3-nitrotyrosine expression in aorta, was associated with increased nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunit NOX-4 protein expression. Endothelial nitric oxide synthase (eNOS) functional inhibition by l-NG-nitroarginine methyl ester, protein expression and activity did not change. In ovariectomized rats, treatment with n-3 PUFA increased n-3 PUFA total content and omega-3 index and decreased n-6:n-3 PUFA ratio in erythrocyte membrane, reversed vascular oxidative stress, endothelial dysfunction, aortic 3-nitrotyrosine and markedly lowered NOX-4 protein expression; eNOS protein expression also increased, paralleled by reversal of inhibitory binding to Caveolin-1, while ex-vivo functional inhibition and NOS synthesis were unchanged. These findings demonstrate in vivo a therapeutic benefit of n-3 PUFA on menopause-associated endothelial dysfunction by reversal of alterations in membrane lipid composition induced by ovariectomy and by reduction of vascular oxidative stress. In this setting they also identify NOX-4 as a potential target to reduce oxidative stress-mediated vascular complications.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt / pharmacology
  • Animals
  • Aorta / drug effects
  • Aorta / metabolism
  • Biomarkers / blood
  • Body Weight / drug effects
  • Caveolin 1 / metabolism
  • Disease Models, Animal
  • Endothelium, Vascular / drug effects*
  • Endothelium, Vascular / physiopathology*
  • Fatty Acids, Omega-3 / pharmacology*
  • Female
  • Free Radical Scavengers / pharmacology
  • Membrane Lipids / chemistry
  • Membrane Lipids / metabolism
  • Menopause / drug effects*
  • Menopause / physiology
  • NADPH Oxidase 4
  • NADPH Oxidases / metabolism
  • Nitric Oxide Synthase Type III / metabolism
  • Ovariectomy
  • Oxidative Stress / drug effects*
  • Rats
  • Rats, Wistar
  • Superoxides / metabolism
  • Vasodilation / drug effects

Substances

  • Biomarkers
  • Cav1 protein, rat
  • Caveolin 1
  • Fatty Acids, Omega-3
  • Free Radical Scavengers
  • Membrane Lipids
  • Superoxides
  • 1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt
  • Nitric Oxide Synthase Type III
  • Nos3 protein, rat
  • NADPH Oxidase 4
  • NADPH Oxidases
  • Nox4 protein, rat