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Effect of Vitamin E on Linoleic Acid-Mediated Induction of Peroxisomal Enzymes in Cultured Porcine Endothelial Cells¹

Bernhard Hennig^*,,2, Gilbert A. Boissonneault^**,, Ching K. Chow^*,, Yin Wang, Daniel H. Matulionis and Howard P. Glauert^*,

^* Department of Nutrition and Food Science ^** Department of Clinical Sciences Department of Anatomy and Neurobiology the Department of Graduate Center for Toxicology, University of Kentucky, Lexington, KY 40506

Linoleic acid decreases endothelial barrier function in culture. We hypothesize that the mechanism may involve induction of peroxisomes, with subsequent generation of hydrogen peroxide, and that vitamin E may protect against barrier function loss by preventing the induction of peroxisomal enzymes. To investigate this hypothesis, we exposed cultured endothelial cells to 0 or 90 µmol/L linoleic acid [18:2(n-6)], with or without 25 µmol/L supplemental vitamin E, for 5 d. The induction of peroxisomes by linoleic acid exposure was determined by measuring cellular peroxisomal ß-oxidation and catalase activity. Vitamin E alone had no effect on ß-oxidation or catalase activity, whereas linoleic acid exposure significantly increased both compared with control values. Vitamin E supplementation prevented induction of peroxisomal ß-oxidation and catalase activity by 18:2. In contrast, cell enrichment with vitamin E had no effect on 18:2-induced accumulation of cytoplasmic lipid-like droplets. These results confirm our hypothesis that the protective effects of vitamin E against fatty acid-mediated endothelial cell injury may be due in part to the ability of vitamin E to prevent the induction of peroxisomal ß-oxidation enzymes and thus the formation of excess hydrogen peroxide.

KEY WORDS: • endothelial cells • vitamin E • fatty acids • peroxisomes • cell injury

¹ Supported in part by grants 1PO1 HL36552 and 1RO1 CA43719 from the National Institutes of Health, a grant from the American Heart Association, Kentucky Affiliate, and the Kentucky Agricultural Experiment Station.

² To whom correspondence and reprint requests should be addressed.

Manuscript received 24 July 1989. Revision accepted 27 November 1989.