Fatty acid–mediated effects on the glutathione redox cycle in cultured endothelial cells

• Published in: The American journal of clinical nutrition Vol. 59; no. 1; pp. 60 - 65
• Main Authors: Toborek, M, Hennig, B
• Format: Journal Article
• Language: English
• Published: Bethesda, MD Elsevier Inc 01-01-1994; American Society for Clinical Nutrition; American Society for Clinical Nutrition, Inc
• Subjects: ACIDE GRAS; ACIDOS GRASOS; Analysis of Variance; Animals; Atherosclerosis (general aspects, experimental research); Biological and medical sciences; Blood and lymphatic vessels; buthionine sulfoximine; Cardiology. Vascular system; Cells, Cultured; Cellular biology; CERDO; CULTIVO DE CELULAS; CULTURE DE CELLULE; DURACION; DUREE; endothehial banncr function; Endothehial cells; Endothelium, Vascular - drug effects; Endothelium, Vascular - metabolism; EPITELIO; EPITHELIUM; fatty acids; Fatty Acids - pharmacology; glutathione; Glutathione - metabolism; glutathione peroxidase; Glutathione Peroxidase - metabolism; glutathione reductase; Glutathione Reductase - metabolism; Hogs; LESION; LESIONES; Medical sciences; Oxidation; Oxidation-Reduction - drug effects; OXIDORREDUCTASAS; OXIRREDUCION; OXYDOREDUCTASE; OXYDOREDUCTION; PEPTIDE; PEPTIDOS; PEROXIDASAS; PEROXYDASE; PORCIN; Swine; Time Factors; fatty acids; glutathione; Endothehial cells; endothehial banncr function; glutathione reductase; buthionine sulfoximine; glutathione peroxidase; Glutathione peroxidase; Endothelial cell; Enzyme; Glutathione reductase (NADPH); Fatty acids; In vitro; Endothelium; Pig; Vertebrata; Mammalia; Peroxidases; Enzymatic activity; Animal; Artiodactyla; Oxidoreductases; Ungulata
• ISSN: 0002-9165; 1938-3207
• DOI: 10.1093/ajcn/59.1.60

Endothelial barrier dysfunction after exposure to fatty acids may be mediated by disturbances in antioxidant protection. To evaluate this hypothesis, components of the glutathione redox cycle such as total, reduced, and oxidized glutathione and glutathione reductase and peroxidase were measured in cultured porcine endothelial cells exposed to 90 µmol/L of stearic acid (18:0), oleic acid (18:lω-9), linoleic acid (18:2ω-6), linolenic acid (18:3ω-3), and/or buthionine sulfoximine (BSO). Treatment with fatty acids caused an initial decrease in glutathione concentrations, which was followed by an increase at later time points. The most marked changes in glutathione redox cycle components were induced by 18:2. BSO increased susceptibility of fatty acid-mediated injury to endothelial monolayers. The results indicate a fundamental role of the glutathione redox cycle in protection against fatty acid-mediated injury to the vascular endothelium.