Transactions of the Association of American Physicians最新文献_第2页

{"title":"Oxidized low-density lipoproteins and endothelium: oral vitamin E supplementation prevents oxidized low-density lipoprotein-mediated vascular injury.","authors":"J Balla, J D Belcher, G Balla, H S Jacob, G M Vercellotti","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Vitamin E supplements may decrease the incidence of myocardial infarction by inhibiting LDL oxidation to atherogenic moieties. We previously reported that hemin is a potent and relevant lipophilic source of iron that can rapidly intercalate into LDL, catalyzing its oxidation and promoting its cytolysis of endothelium. The effects of oral vitamin E on heme-catalyzed LDL oxidation and resulting endothelial damage were studied in 10 volunteers who received daily 800 I.U. of vitamin E with or without vitamin C (1000 mg) for 2 weeks. Prior, during, and 2 weeks after supplementation, plasma LDL was isolated and its number of alpha-tocopherol molecules, resistance to heme-catalyzed oxidation, and ability to damage porcine aortic endothelial cells were assayed. Vitamin E supplementation doubled the lag phase of LDL peroxidation as compared to control (104 +/- 18 vs. 58 +/- 11 min; p < 0.001) accompanied by an increase in alpha-tocopherol content of LDL particles (26 +/- 6 vs. 11 +/- 2 mol/mol; p < 0.001). Most intriguingly, LDL-mediated endothelial cell cytotoxicity was prevented (3 +/- 2% vs. 42 +/- 12%; p < 0.001). After a 2-week washout period, LDL alpha-tocopherol content, the lag time of LDL oxidation, and oxidized LDL-mediated cytolysis all returned to baseline levels. To determine whether supplements of vitamin E and vitamin C beneficially synergize in these effects, we monitored several volunteers on daily vitamin E alone or vitamin C alone. Vitamin E alone (at doses as low as 400 I.U./day) affected all measurements in a manner identical to that when it was taken with vitamin C. Vitamin C alone had no significant effect on these measurements. We conclude: dietary vitamin E supplementation provides cytoprotection against LDL oxidation-mediated endothelial cell injury, but this salutary effect is rapidly lost after supplementation is stopped.</p>","PeriodicalId":23470,"journal":{"name":"Transactions of the Association of American Physicians","volume":"106 ","pages":"128-33"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19030729","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Extracellular matrix gene expression by human keratinocytes and fibroblasts from donors of varying ages. 来自不同年龄供体的人类角质细胞和成纤维细胞的细胞外基质基因表达。

Transactions of the Association of American Physicians Pub Date : 1993-01-01

E M Tan, S Rouda, J Hoffren, Y Q Chen, J Uitto, K Li

引用次数: 0