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National Institute of Environmental Health Sciences

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Your Environment. Your Health.

Publication Detail

Title: Effect of vitamin E on oxysterol- and fatty acid hydroperoxide-induced changes of repair and permeability properties of cultured endothelial cell monolayers.

Authors: Hennig, B; Boissonneault, G A; Fiscus, L J; Marra, M E

Published In Int J Vitam Nutr Res, (1988)

Abstract: Oxidation products of fatty acids (fatty acid hydroperoxides) or of cholesterol (oxysterols) may be atherogenic by being injurious to the vascular endothelium. Vitamin E may protect cells against such injury by acting as an antioxidant and by regulating cell growth and/or repair. As indices of proliferation and growth/repair, synthesis of DNA [3H]thymidine incorporation) and protein ([3H]leucine incorporation), as affected by exposure to linoleic acid hydroperoxide (18:2-OOH), cholestan-3 beta, 5 alpha, 6 beta-triol (Triol), and/or alpha-tocopherol, was determined in confluent vascular endothelial cell cultures. Cell injury was assessed by measuring the passage of albumin through a cultured endothelial monolayer. Exposure to either Triol or 18:2-OOH significantly increased the rate of albumin transfer across endothelial monolayers. Prior enrichment with vitamin E protected endothelial cells from injury by 18:2-OOH but not Triol. Cell exposure to 25 microM vitamin E increased DNA synthesis compared with control cultures. DNA synthesis was also elevated in 18:2-OOH exposed cells, whereas Triol had no effect on cell replication. Prior cell exposure to vitamin E prevented the marked increase in DNA synthesis seen with 18:2-OOH. Protein synthesis was increased by 18:2-OOH, but not by Triol or vitamin E treatment. These results show that 1) both Triol and 18:2-OOH are cytotoxic, 2) vitamin E stimulates cell proliferation, 3) vitamin E protects cells against 18:2-OOH- but not Triol-induced cell injury (i.e., increased permeability to albumin), and 4) endothelial cell damage initiated by 18:2-OOH, but not Triol, stimulates synthesis of DNA and protein in an attempt to divide and repair the injury.(ABSTRACT TRUNCATED AT 250 WORDS)

PubMed ID: 3384583 Exiting the NIEHS site

MeSH Terms: No MeSH terms associated with this publication

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