Hennig B, Boissonneault G A, Chow C K, Wang Y, Matulionis D H, Glauert H P
Department of Nutrition and Food Science, University of Kentucky, Lexington 40506.
J Nutr. 1990 Apr;120(4):331-7. doi: 10.1093/jn/120.4.331.
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 mumols/L linoleic acid [18:2(n-6)], with or without 25 mumols/L supplemental vitamin E, for 5 d. The induction of peroxisomes by linoleic acid exposure was determined by measuring cellular peroxisomal beta-oxidation and catalase activity. Vitamin E alone had no effect on beta-oxidation or catalase activity, whereas linoleic acid exposure significantly increased both compared with control values. Vitamin E supplementation prevented induction of peroxisomal beta-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 beta-oxidation enzymes and thus the formation of excess hydrogen peroxide.
亚油酸会降低培养环境中内皮细胞的屏障功能。我们推测其机制可能涉及过氧化物酶体的诱导，随后产生过氧化氢，并且维生素E可能通过阻止过氧化物酶体酶的诱导来防止屏障功能丧失。为了研究这一假设，我们将培养的内皮细胞暴露于0或90μmol/L的亚油酸[18:2(n - 6)]中，添加或不添加25μmol/L的补充维生素E，持续5天。通过测量细胞过氧化物酶体β - 氧化和过氧化氢酶活性来确定亚油酸暴露对过氧化物酶体的诱导作用。单独的维生素E对β - 氧化或过氧化氢酶活性没有影响，而与对照值相比，亚油酸暴露显著增加了两者。补充维生素E可防止18:2诱导的过氧化物酶体β - 氧化和过氧化氢酶活性。相反，用维生素E富集细胞对18:2诱导的细胞质脂质样小滴积累没有影响。这些结果证实了我们的假设，即维生素E对脂肪酸介导的内皮细胞损伤的保护作用可能部分归因于维生素E阻止过氧化物酶体β - 氧化酶诱导从而防止过量过氧化氢形成的能力。
