Vitamins C and E: Beneficial effects from a mechanistic perspective

Abstract

The mechanistic properties of two dietary antioxidants that are required by humans, vitamins C and E, are discussed relative to their biological effects. Vitamin C (ascorbic acid) is an essential cofactor for α-ketoglutarate-dependent dioxygenases. Examples are prolyl hydroxylases, which play a role in the biosynthesis of collagen and in down-regulation of hypoxia-inducible factor (HIF)-1, a transcription factor that regulates many genes responsible for tumor growth, energy metabolism, and neutrophil function and apoptosis. Vitamin C-dependent inhibition of the HIF pathway may provide alternative or additional approaches for controlling tumor progression, infections and inflammation. Vitamin E (α-tocopherol) functions as an essential lipid soluble antioxidant, scavenging hydroperoxyl radicals in lipid milieu. Human symptoms of vitamin E deficiency suggest that its antioxidant properties play a major role in protecting erythrocyte membranes and nervous tissues. As an antioxidant, vitamin C provides protection against oxidative stress-induced cellular damage by scavenging of reactive oxygen species, vitamin E-dependent neutralization of lipid hydroperoxyl radicals, and by protecting proteins from alkylation by electrophilic lipid peroxidation products. These bioactivities bear relevance to inflammatory disorders. Vitamin C plays also a role in the function of endothelial nitric oxide synthase (eNOS) by recycling the eNOS cofactor, tetrahydrobiopterin, which is relevant to arterial elasticity and blood pressure regulation. Evidence from plants supports a role for vitamin C in the formation of covalent adducts with electrophilic secondary metabolites. Mechanism-based effects of vitamin C and E supplementation on biomarkers and on clinical outcomes from randomized, placebo-controlled trials are emphasized in this review.

Effects of food allergy on the dietary habits and intake of primary schools’ Cypriot children

“…Vitamin E intake was significantly lower in food allergic children, probably due to the lower consumption of vegetable oils. Vitamin E is associated with optimal health and cell protection from oxidative damage (24), whereas it can have a protective role together with other antioxidants against allergies (25). The current study revealed several significant differences between nutrient intake and food variety among healthy and food allergic elementary school children, despite the low rates of response.…”

Fast Retrograde Signaling in Response to High Light Involves Metabolite Export, MITOGEN-ACTIVATED PROTEIN KINASE6, and AP2/ERF Transcription Factors in Arabidopsis

“…All selected genes showed significantly altered expression levels in the erf6 mutant (quantitative PCR, n = 3 independent experiments with duplicate determinations, mean 6 SE, asterisks indicate significant difference, Student's t test P < 0.05). (Gill and Tuteja, 2010;Traber and Stevens, 2011). Hence, measurements of tocopherol levels during a L→H transition might provide more information about involved signaling pathways and acclimation processes to H-light.…”

Risk of Severe Influenza Infection: Hypercytokinemia Gene Polymorphisms and Related Plasma Proteome in Canadian Young Adults

“…Moreover, γ-tocopherol, which is more abundant in the American diet than other forms of vitamin E (e.g., α-tocopherol), was non-significantly elevated in subjects with ≥ three-risk genotypes, but was significantly higher in the AA risk genotype of the CCL1 rs2282691. The observation that the number of risk genotypes is correlated with the level of afamin, a vitamin E-binding glycoprotein that plays a role in vitamin E transport [21], may shed some light on the potential relationship between the antioxidant characteristics of vitamin E and risk of severe clinical IAV [31,32,37]. Furthermore, consideration of vitamin E intake may also be beneficial for women who possess the cytokine risk genotypes given their overall lower levels of δ-tocopherol and γ-tocopherol compared with men.…”

“…Attenuation of the innate immune system during infection can be genetically-and/or environmentally-mediated leading to the overproduction of pro-inflammatory cytokines such as ILs, TNF-α, IFN-γ and TGF-β [17,18]. This response is known to occur in a number of infectious diseases [30][31][32] including IAV [14,15,17,18], leading to the ensuing delayed clearance of viral load, vasculopathy, hemorrhage and tissue [14,15,17,18,33,34]. The results of the present study suggest that polymorphisms in the hypercytokinemia genes are associated with a proteomic profile linked to innate immunity activation (e.g., haptoglobin β chain), the modulation of the complement pathway, increased levels of acute phase reactants (e.g., CRP and hemopexin) and altered levels of L-selectin influencing the overall function of leukocytes.…”