Vitamin E, LDL, and EndotheliumBrief Oral Vitamin Supplementation Prevents Oxidized LDL‐Mediated Vascular Injury In Vitro
作者:
John Belcher,
Jozsef Balla,
Gyorgy Balla,
David Jacobs,
Myron Gross,
Harry Jacob,
Gregory Vercellotti,
期刊:
Arteriosclerosis and Thrombosis: A Journal of Vascular Biology
(OVID Available online 1993)
卷期:
Volume 13,
issue 12
页码: 1779-1789
ISSN:1049-8834
年代: 1993
出版商: OVID
关键词: vitamin E;LDL;oxidized LDL;vitamin C;atherosclerosis;heme;iron
数据来源: OVID
摘要:
In previously reported in vitro studies, we found that heme, a physiologically widespread hydrophobic iron compound, can rapidly generate oxidized low-density lipoprotein (LDL), which then becomes cytotoxic to cultured vascular endothelial cells; both LDL oxidation and endothelial cytotoxicity were inhibited by incubation with exogenous a-tocopherol (vitamin E) or ascorbic acid (vitamin C). Seeking relevance to in vivo conditions, we performed a study in which 10 human volunteers were given daily antioxidant supplements of 800 IU of DL-<x-tocopherol acetate alone or in combination with 1000 mg of ascorbic acid for 2 weeks. LDL resistance to heme oxidation ex vivo, as measured by the lag time for conjugated-diene formation, increased by as much as threefold from a mean±SD of 58±11 to 104±18 minutes (p<.001); LDL a-tocopherol increased from 11 ±2 to 26±6 molecules per LDL particle (p<.001); and most impressively, cytotoxicity to porcine aortic endothelial cells incubated with LDL conditioned with heme plus H2O2or with copper was completely prevented (cytotoxicity before supplementation was 42 + 12%, decreasing after supplementation to 3±2%,p<.001). These measurements reverted to their presupplement levels within 2 weeks after participants stopped taking antioxidant supplements and were reproduced in 4 subjects taking 800 IU of DL-a-tocopherol acetate supplements alone but not in the same subjects taking 1000 mg ascorbic acid supplements alone. In conclusion, oral vitamin E supplementation increases LDL or-tocopherol content, increases LDL resistance to oxidation, and decreases the cytotoxicity of oxidized LDL to cultured vascular endothelial cells.
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