Effect of vitamins C and E on progression of transplant-associated arteriosclerosis: a randomised trial

Fang, Juemin; Kinlay, Scott; Beltrame, John F.

doi:10.1016/s1062-1458(02)00781-x

Cited by 100 publications

(128 citation statements)

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“…For example, daily supplementation of 400 IU of vitamin E orally twice daily and 500 mg of vitamin C orally twice daily can achieve serum level of 103 and 65 M, respectively (10). This opens up the possibility of using vitamintreated DC for the induction of tolerance to auto-or alloantigens.…”

Section: Discussionmentioning

confidence: 99%

“…Vitamin E is efficiently reduced from its free radical form (tocotrienoxyl or tocopheroxyl) that arises after quenching lipid radicals to return back to its native state (tocotrienol and tocopherol) by vitamin C. Vitamin C can regenerate vitamin E directly, while thiol antioxidants, such as glutathione and lipoic acid, can also regenerate vitamin E indirectly via vitamin C. Under conditions in which these systems act to keep the steady state concentration of vitamin E radicals low, the loss or consumption of vitamin E is prevented. It has been reported that the concurrent use of vitamin C can augment the effect of vitamin E (7) in the treatment of cardiovascular (8), neurological diseases (9), and chronic transplant rejection (10). For these reasons, we used combinations of vitamins C and E (in the form of ␣-TOH) when investigating their antioxidant effect on dendritic cells (DCs).…”

Section: Ietary Antioxidants (Eg Vitamin E (Including ␣-Tocoph-mentioning

confidence: 99%

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Inhibition of NF-κB and Oxidative Pathways in Human Dendritic Cells by Antioxidative Vitamins Generates Regulatory T Cells

Tan

Sagoo

Chan

et al. 2005

The Journal of Immunology

198

159

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Dendritic cells (DCs) are central to T cell immunity, and many strategies have been used to manipulate DCs to modify immune responses. We investigated the effects of antioxidants ascorbate (vitamin C) and α-tocopherol (vitamin E) on DC phenotype and function. Vitamins C and E are both antioxidants, and concurrent use results in a nonadditive activity. We have demonstrated that DC treated with these antioxidants are resistant to phenotypic and functional changes following stimulation with proinflammatory cytokines. Following treatment, the levels of intracellular oxygen radical species were reduced, and the protein kinase RNA-regulated, eukaryotic translation initiation factor 2α, NF-κB, protein kinase C, and p38 MAPK pathways could not be activated following inflammatory agent stimulation. We went on to show that allogeneic T cells (including CD4+CD45RO, CD4+CD45RA, and CD4+CD25− subsets) were anergized following exposure to vitamin-treated DCs, and secreted higher levels of Th2 cytokines and IL-10 than cells incubated with control DCs. These anergic T cells act as regulatory T cells in a contact-dependent manner that is not dependent on IL-4, IL-5, IL-10, IL-13, and TGF-β. These data indicate that vitamin C- and E-treated DC might be useful for the induction of tolerance to allo- or autoantigens.

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Section: Discussionmentioning

confidence: 99%

Section: Ietary Antioxidants (Eg Vitamin E (Including ␣-Tocoph-mentioning

confidence: 99%

Inhibition of NF-κB and Oxidative Pathways in Human Dendritic Cells by Antioxidative Vitamins Generates Regulatory T Cells

Tan

Sagoo

Chan

et al. 2005

The Journal of Immunology

198

159

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“…Although the preponderance of clinical trial evidence has not shown beneficial effects of antioxidant supplements, evidence from some smaller studies documents a benefit of ␣-tocopherol (Cambridge Heart AntiOxidant Study, 13 Secondary Prevention with Antioxidants of Cardiovascular disease in End-stage renal disease study), 15 ␣-tocopherol and slow-release vitamin C (Antioxidant Supplementation in Atherosclerosis Prevention study), 16 and vitamin C plus vitamin E (Intravascular Ultrasonography Study) 17 on cardio-vascular end points. To complicate matters, there is some evidence of potentially adverse effects of antioxidant supplements on CVD as assessed by angiographic end points.…”

mentioning

confidence: 99%

Antioxidant Vitamin Supplements and Cardiovascular Disease

Kris‐Etherton¹,

Lichtenstein²,

Howard³

et al. 2004

Circulation

347

183

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“…Tocopherol treatment was found to lower the risk of coronary events, mainly through a reduction in non-fatal myocardial infarction; CVD deaths were not found to be significantly altered. Another study has found that a-tocopherol supplementation suppresses restenosis in surgically-induced atherosclerosis (35) , although this outcome has not been found in all studies.…”

Section: Intervention Trialsmentioning

confidence: 89%

Antioxidants and CVD

Bruckdorfer

2008

Proc. Nutr. Soc.

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The involvement of free radicals and reactive oxygen and nitrogen species in the pathology of inflammatory and degenerative disease has been widely accepted, although the centrality of these species to the outcome of these diseases is still a matter for debate. In the case of CVD, and particularly the development of the atherosclerotic plaque, the oxidation of LDL is of particular importance and appears to explain many of the events that occur during the life history of the plaque. The corollary of this situation is that antioxidants must be a benign force to protect the population from the modern scourge of heart disease. In fact, recent evidence from intervention studies with large doses of the antioxidant vitamins and other antioxidants in foods has been very disappointing. Here, the background for the belief that antioxidants ought to be beneficial is examined and an attempt made to explain why the results of these intervention studies have been unsuccessful. It is agreed that a diet rich in fruit and vegetables is protective for both CVD and cancer, but the explanation for this effect may not necessarily lie with the presence of antioxidants.

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Effect of vitamins C and E on progression of transplant-associated arteriosclerosis: a randomised trial

Cited by 100 publications

References 0 publications

Inhibition of NF-κB and Oxidative Pathways in Human Dendritic Cells by Antioxidative Vitamins Generates Regulatory T Cells

Inhibition of NF-κB and Oxidative Pathways in Human Dendritic Cells by Antioxidative Vitamins Generates Regulatory T Cells

Antioxidant Vitamin Supplements and Cardiovascular Disease

Antioxidants and CVD

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