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Prevention of atherosclerosis by alpha-tocopherol in smooth muscle cells by a mechanism involving signal transduction modulation

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dc.contributor.authorsOzer, NK; Sirikci, O; Taha, S; Engin, NK; Boscoboinik, D; Clement, S; Stocker, A; Azzi, A
dc.contributor.editorOzben, T
dc.date.accessioned2022-03-12T15:58:09Z
dc.date.available2022-03-12T15:58:09Z
dc.date.issued1998
dc.description.abstractalpha-Tocopherol, the biologically most active form of Vitamin E, decreases in a concentration dependent way, proliferation of smooth muscle cells. At the same concentrations (10-50 mu M) it induces inhibition of protein kinase C activity. Proliferation and protein kinase C inhibition by alpha-tocopherol, the lack of inhibition by beta-tocopherol and the prevention by beta-tocopherol indicate that the mechanism involved is not related to the radical-scavenging properties of these two molecules, which are essentially equal. All-rac-alpha-tocopherol is less potent than RRR-alpha-tocopherol on smooth muscle cell proliferation. probucol(10-50 mu M), a potent lipophilic antioxidant, does not inhibit smooth muscle cell proliferation and protein kinase C activity. In rabbit studies, atherosclerosis was induced by a 2% cholesterol-containing, vitamin E poor-diet. Six different groups of rabbits each were received vitamin E, probucol; probucol plus vitamin E. After 4 weeks, aortas were analysed for protein kinase C activity. Their media smooth muscle cells exhibited an increase in protein kinase C activity. Vitamin E fully prevented cholesterol induced atherosclerotic lesions and the induction of protein kinase C activity. Probucol was not effective in preventing both cholesterol induced atherosclerotic lesions and the induction of protein kinase C activity. These results show that the protective effect of vitamin E against hypercholesterolemic atherosclerosis is not produced by an other antioxidant such as probucol and therefore may not be linked to the antioxidant properties of this vitamin. The effects observed at the level of smooth muscle cells ex-vivo and cell culture suggest an involvement of signal transduction events on the onset of atherosclerosis. It is at this level that the protective effect of vitamin E against atherosclerosis is exerted.
dc.identifier.doidoiWOS:000073945700029
dc.identifier.isbn0-306-45813-6
dc.identifier.issn0258-1213
dc.identifier.urihttps://hdl.handle.net/11424/223951
dc.identifier.wosWOS:000073945700029
dc.language.isoeng
dc.publisherPLENUM PRESS DIV PLENUM PUBLISHING CORP
dc.relation.ispartofFREE RADICALS, OXIDATIVE STRESS, AND ANTIOXIDANTS: PATHOLOGICAL AND PHYSIOLOGICAL SIGNIFICANCE
dc.relation.ispartofseriesNATO ADVANCED SCIENCE INSTITUTES SERIES, SERIES A, LIFE SCIENCES
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.titlePrevention of atherosclerosis by alpha-tocopherol in smooth muscle cells by a mechanism involving signal transduction modulation
dc.typeconferenceObject
dspace.entity.typePublication
local.avesis.id37a1430d-8064-492b-8033-1c0aafb853c9
local.conference.dateMAY 24-JUN 04, 1997
local.conference.locationANTALYA, TURKEY
local.conference.sponsorNATO, Sci Affairs Div
local.conference.titleNATO Advanced Study Institute on Free Radicals, Oxidative Stress, and Antioxidants - Pathological and Physiological Significance
local.import.packageSS15
local.indexed.atWOS
local.journal.numberofpages10
oaire.citation.endPage342
oaire.citation.startPage333
oaire.citation.titleFREE RADICALS, OXIDATIVE STRESS, AND ANTIOXIDANTS: PATHOLOGICAL AND PHYSIOLOGICAL SIGNIFICANCE
oaire.citation.volume296

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