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Vitamin a Decreases Cytotoxicity of Oxidized Low-Density Lipoprotein in Patients With Atherosclerosis Publisher Pubmed



Mahmoudi MJ1 ; Sabooryaraghi AA2 ; Zabetiantarghi F2 ; Siassi F3 ; Zarnani AH4, 5 ; Eshraghian MR6 ; Shokri F7 ; Rezaei N8, 9 ; Kalikias Y2 ; Mahmoudi M2
Authors
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Authors Affiliations
  1. 1. Division of Cardiology, Department of Internal Medicine, Tehran University of Medical Sciences, Tehran, Iran
  2. 2. Department of Cellular Molecular Nutrition, School of Nutritional Sciences and Dietetics, Tehran University of Medical Sciences, Tehran, Iran
  3. 3. Department of Community Nutrition, School of Nutritional Sciences and Dietetics, Tehran University of Medical Sciences, Tehran, Iran
  4. 4. Nanobiotechnology Research Center, Avicenna Research Institute, ACECR, Tehran, Iran
  5. 5. Immunology Research Center, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran
  6. 6. Department of Biostatistics, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran
  7. 7. Department of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran
  8. 8. Molecular Immunology Research Center, Department of Immunology, Tehran University of Medical Sciences, Tehran, Iran
  9. 9. Research Group for Immunodeficiencies, Pediatrics Center of Excellence, Tehran University of Medical Sciences, Tehran, Iran

Source: Immunological Investigations Published:2016


Abstract

Background: Oxidized low-density lipoprotein (ox-LDL) is implicated in initiation and progression of atherosclerosis. Previously, we found that ox-LDL increases vulnerability of peripheral blood mononuclear cells (PBMCs) in atherosclerotic patients compared to controls. Vitamin A induces proliferation of PBMCs. The aim of this study was to determine the effect of Vitamin A supplementation on PBMC survival against LDL and different doses of ox-LDL.Method: In this double-blind placebo-controlled trial, we recruited 35 atherosclerotic patients and 38 healthy controls and randomly allocated them into placebo and Vitamin A groups, which received either placebo or 25,000 IU/day of Vitamin A for 3 months. PBMCs were isolated, cultured, and stimulated by 1 μg/mL LDL as well as 1 μg/mL and 50 μg/mL ox-LDL. The stimulation indexes (SIs) of PBMCs were calculated to identify cell viability. Additionally, the circulating ox-LDL levels were measured by ELISA.Results: Viability of PBMCs stimulated by 50 μg/mL ox-LDL significantly increased following Vitamin A supplementation in patients (p < 0.01). The levels of circulating ox-LDL were not changed by Vitamin A treatment. Ox-LDL levels were strongly and positively correlated to SI of PBMCs stimulated by 1 μg/mL LDL and1 μg/mL ox-LDL in all groups.Conclusion: Vitamin A decreases cytotoxicity of high-dose ox-LDL and improves PBMC viability. The protective effect of Vitamin A is not mediated by an antioxidative mechanism, but may instead have been due to intracellular protection of the apoptotic machinery or induction of proliferation of the cells. Higher levels of ox-LDL increase PBMC irritability in all participants. © 2015 Taylor & Francis.