Vitamin E: The shrew waiting to be tamed

Brigelius‐Flohé, Regina

doi:10.1016/j.freeradbiomed.2008.12.007

Cited by 231 publications

(184 citation statements)

References 177 publications

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“…There are many studies demonstrating that VE protects cell membranes by preventing LPO. α-Tocopherol reacts with peroxyl radicals depending on its methylation state of the chromanol ring and the saturation grade of the side chain, forming tocopheroxyl radicals (Brigelius-Flohe, 2009). Tocopheroxyl radicals are converted to tocopherols by reacting with ascorbate (May et al, 1998).…”

Section: Discussionmentioning

confidence: 99%

Protective role of vitamins C and E in diclorvos-induced oxidative stress in human erythrocytes in vitro

et al. 2013

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Organophosphate (OP) pesticides such as dichlorvos (DDVP) intoxication has been shown to produce oxidative stress due to the generation of free radicals, which alter the antioxidant defense system in erythrocytes. In this study, the eff ects of DDVP (1, 10, 100 μM) or DDVP + vitamin C (VC; 10 μM) or vitamin E (VE; 30 μM), on the levels of malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) activities in human erythrocytes were examined in vitro. There were no statistical diff erences between all groups for 1 μM concentration of DDVP. Treatment with DDVP alone produced an increase in the level of MDA and decreased activities of antioxidant enzymes (P < 0.05). Groups treated with vitamins and DDVP showed protective eff ects of vitamins against DDVP-induced changes in antioxidant enzyme activity and lipid peroxidation (LPO) (10 μM). At 100 μM concentration of DDVP vitamins had no eff ect on DDVP-induced toxicity. The results show that administration of DDVP resulted in the induction of erythrocyte LPO and alterations in antioxidant enzyme activities, suggesting that reactive oxygen species (ROS) may be involved in the toxic eff ects of DDVP. Also the data show that the plasma level of VC and VE may ameliorate OP-induced oxidative stress by decreasing LPO in erythrocytes at certain doses of OP pesicides.

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Section: Discussionmentioning

confidence: 99%

Protective role of vitamins C and E in diclorvos-induced oxidative stress in human erythrocytes in vitro

et al. 2013

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“…The biological function of a-tocopherol is made more interesting should we consider the possibility of mechanisms of action independent of antioxidant activity. Indeed, the effect of a-tocopherol on membrane resident proteins and enzymes, signaling cascades, and gene expression, may be related to its contribution to membrane structure and dynamics, and thus modulation of membranedependent signaling mechanisms such as protein and lipid kinases [96][97][98]. We have described here how our work using 2 H-NMR and neutron diffraction will enable a more detailed understanding of how tocopherol behaves when immersed in phospholipid bilayers of increasing polyunsaturation.…”

Section: Is All Of This Relevant For Understanding the Biological Actmentioning

confidence: 99%

The location and behavior of α‐tocopherol in membranes

Atkinson

Harroun

Wassall

et al. 2010

Molecular Nutrition Food Res

172

128

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Vitamin E (a-tocopherol) has long been recognized as the major antioxidant in biological membranes, and yet many structurally related questions persist of how the vitamin functions. For example, the very low levels of a-tocopherol reported for whole cell extracts question how this molecule can successfully protect the comparatively enormous quantities of PUFAcontaining phospholipids found in membranes that are highly susceptible to oxidative attack. The contemporary realization that membranes laterally segregate into regions of distinct lipid composition (domains), we propose, provides the answer. We hypothesize a-tocopherol partitions into domains that are enriched in polyunsaturated phospholipids, amplifying the concentration of the vitamin in the place where it is most needed. These highly disordered domains depleted in cholesterol are analogous, but organizationally antithetical, to the wellstudied lipid rafts. We review here the ideas that led to our hypothesis. Experimental evidence in support of the formation of PUFA-rich domains in model membranes is presented, focusing upon docosahexaenoic acid that is the most unsaturated fatty acid commonly found. Physical methodologies are then described to elucidate the nature of the interaction of a-tocopherol with PUFA and to establish that the vitamin and PUFA-containing phospholipids co-localize in non-raft domains.

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“…As α-TTP is also abundantly expressed in the placenta, the importance of α-TOH in preventing fetus resorption is evident [98] . Furthermore, α-TTP is also expressed in several other tissues [76] , such as rat brain, spleen, lung and kidney [99] , the pregnant mouse uterus [100] , retina [101] and central nervous system [21] , suggesting an ubiquitous role for α-TTP in intra-organ trafficking [102] . Hosomi et al [103] estimated the relative affinities of α-TTP to the different vitamin E forms and stereoisomers starting from RRR-α-TOH set to 100%: β-TOH (38%), α-T3 (12%), SRR-α-TOH (11%), γ-TOH and trolox (9%) followed by δ-TOH, α-TOH acetate and α-TOH quinone with 2%.…”

Section: Intracellular Binding Proteins α -Tocopherol Transfer Proteinmentioning

confidence: 99%

Complexity of vitamin E metabolism

Schmölz¹,

Birringer²,

Lorkowski³

et al. 2016

WJBC

176

138

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Bioavailability of vitamin E is influenced by several factors, most are highlighted in this review. While gender, age and genetic constitution influence vitamin E bioavailability but cannot be modified, life-style and intake of vitamin E can be. Numerous factors must be taken into account however, i.e. , when vitamin E is orally administrated, the food matrix may contain competing nutrients. The complex metabolic processes comprise intestinal absorption, vascular transport, hepatic sorting by intracellular binding proteins, such as the significant α-tocopherol-transfer protein, and hepatic metabolism. The coordinated changes involved in the hepatic metabolism of vitamin E provide an effective physiological pathway to protect tissues against the excessive accumulation of, in particular, non-α-tocopherol forms. Metabolism of vitamin E begins with one cycle of CYP4F2/CYP3A4-dependent ω-hydroxylation followed by five cycles of subsequent β-oxidation, and forms the water-soluble end-product carboxyethylhydroxychroman. All known hepatic metabolites can be conjugated and are excreted, depending on the length of their sidechain, either via urine or feces. The physiological handling of vitamin E underlies kinetics which vary between the different vitamin E forms. Here, saturation of the side-chain and also substitution of the chromanol ring system are important. Most of the metabolic reactions and processes that are involved with vitamin E are also shared by other fat soluble vitamins. Influencing interactions with other nutrients such as vitamin K or pharmaceuticals are also covered by this review. All these processes modulate the formation of vitamin E metabolites and their concentrations in tissues and body fluids. Differences in metabolism might be responsible for the discrepancies that have been observed in studies performed in vivo and in vitro using vitamin E as a REVIEW

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Vitamin E: The shrew waiting to be tamed

Cited by 231 publications

References 177 publications

Protective role of vitamins C and E in diclorvos-induced oxidative stress in human erythrocytes in vitro

Protective role of vitamins C and E in diclorvos-induced oxidative stress in human erythrocytes in vitro

The location and behavior of α‐tocopherol in membranes

Complexity of vitamin E metabolism

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