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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vitamin E (alpha-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 alpha-tocopherol reported for whole cell extracts question how this molecule can successfully protect the comparatively enormous quantities of PUFA-containing 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 alpha-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 well-studied 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 alpha-tocopherol with PUFA and to establish that the vitamin and PUFA-containing phospholipids co-localize in non-raft domains.
Mol Nutr Food Res 2010 May
PMID:The location and behavior of alpha-tocopherol in membranes. 2016 46

Vitamin E is composed of closely related compounds, including tocopherols and tocotrienols. Studies of the last decade provide strong support for a specific role of alpha-tocopherol in cell signalling and the regulation of gene expression. It produces significant effects on inflammation, cell proliferation and apoptosis that are not shared by other vitamin E isomers with similar antioxidant properties. The different behaviours of vitamin E isomers might relate, at least in part, to the specific effects they exert at the plasma membrane. alpha-Tocopherol is not randomly distributed throughout the phospholipid bilayer of biological membranes, and as compared with other isomers, it shows a propensity to associate with lipid rafts. Distinct aspects of vitamin E transport and metabolism is discussed with emphasis on the interaction between alpha-tocopherol and lipid rafts and the consequences of these interactions on cell metabolism.
Mol Nutr Food Res 2010 May
PMID:Vitamin E transport, membrane incorporation and cell metabolism: Is alpha-tocopherol in lipid rafts an oar in the lifeboat? 2016 47

Vitamin E is known as the most important lipid antioxidant and is widely used to prevent age-associated diseases. Despite increasing knowledge about human vitamin E metabolism, little is known to justify its widespread use. As meta-analyses revealed even harmful effects of high vitamin E doses, a profound understanding of vitamin E metabolism is mandatory. By recent advances in analytical methodology, new metabolites with distinct physicochemical and biological properties were discovered. This review covers current methods to analyze vitamin E metabolites in biological samples. Special emphasis is laid on analytical applications for the identification and quantification of metabolites with a modified hydroxychromanol ring or a truncated side chain.
Mol Nutr Food Res 2010 May
PMID:Analysis of vitamin E metabolites in biological specimen. 2016 85

A very low level of intra-erythrocytic calcium content is very important for normal physiology of cells. In the present study, our main objective was to investigate the effects of atrazine toxicity on Ca(2+) homeostasis and modulation by vitamin E. Experimental animals were orally administered atrazine (300 mg kg(-1) body weight, daily) and vitamin E (100 mg kg(-1) body weight, daily). All studies were carried out for 7, 14, and 21 days in male Wistar rats. Erythrocyte membranes were prepared and were analyzed for lipid peroxidation (LPO) and membrane bound ATPases. Furthermore, Ca(2+) homeostasis was evaluated in erythrocytes. The present findings indicated that atrazine exposure induced oxidative stress which was associated with significant increase in lipid peroxidation (P < 0.05). Vitamin E treatment on the other hand significantly lowered the atrazine-induced lipid peroxidation. The increased LPO following atrazine exposure was accompanied by significant decrease in ATPases (P < 0.05) and disturbed Ca(2+) homeostasis. Furthermore, vitamin E treatment had a beneficial effect by partially restoring ATPases and Ca(2+) homeostasis. The current findings suggest that atrazine exerts its toxic effect by increasing LPO, altering the activity of membrane bound enzymes and disturbing Ca(2+) homeostasis. Vitamin E treatment ameliorated the toxic effects of atrazine suggesting its role as a potential antioxidant.
Mol Cell Biochem 2010 Jul
PMID:Alterations in Ca2+ homeostasis in rat erythrocytes with atrazine treatment: positive modulation by vitamin E. 2019 5

Vitamin E refers to a family of several compounds that possess a similar chemical structure comprising a chromanol ring with a 16-carbon side chain. The degree of saturation of the side chain, and positions and nature of methyl groups designate the compounds as tocopherols or tocotrienols. Vitamin E compounds have antioxidant properties due to a hydroxyl group on the chromanol ring. Recently, it has been suggested that vitamin E may also regulate signal transduction and gene expression. We previously reported that lifelong dietary vitamin E (alpha-tocopherol) supplementation significantly increased median lifespan in C57BL/6 mice by 15%. This lifespan extension appeared to be independent of any antioxidant effect. Employing a transcriptional approach, we suggest that this increase in lifespan may reflect an anti-cancer effect via induction of the P21 signalling pathway, since cancer is the major cause of death in small rodents. We suggest that the role of this pathway in life span extension following supplementation of vitamin E now requires further investigation.
Mol Nutr Food Res 2010 May
PMID:Vitamin E supplementation and mammalian lifespan. 2020 92

Vitamin E is an essential fat-soluble micronutrient for higher mammals and functions as an antioxidant for lipids and also as a regulator of gene expression and a modulator of cell signaling and proliferation. To exert its physiological functions, vitamin E must achieve an appropriate disposition throughout the body via several processes, such as intestinal absorption, uptake and efflux in peripheral tissues and biliary secretion. In this review, we mainly discuss membrane proteins involved in these transport processes (ATP-binding cassette transporter A1, scavenger receptor class B type I, Niemann-Pick C1-like 1 and multidrug resistance 3) and vitamin E-mediated regulation of their expression.
Mol Nutr Food Res 2010 May
PMID:Molecular mechanisms of membrane transport of vitamin E. 2020 93

The term Vitamin E is utilized to describe eight molecules, subdivided into two groups, tocopherols and tocotrienols (TTs). It has been shown that specific TTs affect the growth of several lines of tumour cells, and that this activity is not shared by tocopherols. In agreement with these observations, a TTs-rich fraction from palm oil (PTRF) was reported to inhibit proliferation and induce apoptosis in several cancer cells. However, the molecular mechanism involved in TTs activity is still unclear. We have recently proposed that TTs pro-apoptotic activity involves estrogen receptor beta (ERbeta) signalling. In this study, we report that, in MCF-7 breast cancer cell, expressing both ERalpha and ERbeta, PTRF treatment increases ERbeta nuclear translocation, as demonstrated by immunofluorescence experiments and significantly inhibits ERalpha expression (-458.91-fold of change) and complete disappearing of the protein from the nucleus. Moreover, PTRF treatment induces ER-dependent genes expression (macrophage inhibitory cytokine-1, early growth response-1 and Cathepsin D) which is inhibited by the ER inhibitor, ICI 182.780, and induces DNA fragmentation. Finally, cDNA-array experiments suggest that the activation of specific pathways in cells treated with gamma-TT with respect to alpha-TT. Our data suggest a novel potential molecular mechanism for TTs activity.
Mol Nutr Food Res 2010 May
PMID:Tocotrienols activity in MCF-7 breast cancer cells: involvement of ERbeta signal transduction. 2030 77

Vitamin E is one of the most important lipid-soluble antioxidants to occur in plants and animals for cellular protection against lipid peroxidation. An essential adaptation to low temperature is the elaboration of high levels of unsaturated fatty acids in the composition of cellular membranes, which is necessary to maintain functional membrane fluidity. Increasing the content of lipid unsaturation, however, occurs at the expense of enhancing the vulnerability of cellular membranes to oxidative damage. First isolated from salmon eggs, cold-water marine organisms were found to produce, or acquire, a specific vitamin E homologue, named "marine-derived tocopherol" (MDT), having an unusual methylene unsaturation at its isoprenoid-chain terminus. In this overview we compare the antioxidant composition of tropical, temperate and polar fishes, present provisional evidence that MDT is produced at the primary food chain, and provide empirical confirmation that the enhanced reactivity of MDT at low temperature is attributed to its greater rate of diffusion in viscous lipids at low temperatures. This claim of biochemical adaptation is supported by a unique model of diffusion-limited reactivity that mimics changes in the ratio of the MDT/alpha-tocopherol rate constants at diminishing levels of radical flux in viscous media at low temperature. We offer in conclusion future outlooks to research on antioxidant protection in cold-water ectotherms.
Comp Biochem Physiol B Biochem Mol Biol 2010 Oct
PMID:Vitamin E protection in the biochemical adaptation of marine organisms to cold-water environments. 2042 25

Hypercholesterolemia induces oxidative stress, which is known to have adverse effects on the integrity of cells. Hence, hypercholesterolemia may have adverse effects on the hemopoietic system. Vitamin E, an antioxidant, is being used by normo- and hypercholesterolemic subjects. It is, however, not known if vitamin E has any beneficial or adverse effects on the hemopoietic system. The objectives of this study are to determine if (i) hypercholesterolemia has any adverse effects on the hemopoietic system [red blood cell (RBC) count, mean corpuscular volume (MCV), red blood cell distribution width (RDW), hematocrit (Hct), hemoglobin (Hb), mean corpuscular hemoglobin (MCH), MCH concentration (MCHC), white blood cell (WBC), and platelet counts, and mean platelet volume (MPV)], and (ii) vitamin E has any effect on the hemopoietic system in hypercholesterolemia. Blood samples were collected before and at various intervals during a high cholesterol diet (0.25% cholesterol) for 2 and 4 months, and while on high cholesterol diet with vitamin E (2 months) following a high cholesterol diet (2 months). Serum cholesterol was measured on an automated Clinical System Analyzer and hemopoietic parameters were measured on an automated Cell-dyn-4000. The results show that hypercholesterolemia decreased RBC count, Hct and Hb, increased MCV, RDW, MCH, and MCHC, and had no effect on WBC and platelet counts, and MPV. Vitamin E did not affect any of the parameters of the hemopoietic system. In conclusion, hypercholesterolemia of short duration has adverse effects on certain elements of the hemopoietic system. Vitamin E does not affect the hemopoietic system during hypercholesterolemia.
Mol Cell Biochem 2010 Oct
PMID:Effect of chronic administration of vitamin E on the hemopoietic system in hypercholesterolemia. 2052 44

The present study investigates the antioxidative effects of vitamin E and curcumin against L-thyroxine (T(4))-induced oxidative stress in renal cortex of adult male rats. Rats were made hyperthyroid by administration of L-thyroxine (0.0012%) in their drinking water for 30 days. Vitamin E (200 mg/kg body weight/day) and curcumin (30 mg/kg body weight/day) were supplemented singly or in combination orally for 30 days along with L-thyroxine treatment. The elevated level of oxidative stress parameters (lipid peroxidation and protein carbonylation) and decline level of small antioxidant molecules (reduced glutathione and ascorbic acid) in renal cortex of T(4)-treated rats were restored back by supplementation of vitamin E or/and curcumin. Increased superoxide dismutase and catalase activities in kidney cortex of T(4)-treated rats were ameliorated in response to vitamin E or/and curcumin treatment. The elevated translated product of Cu/Zn-SOD, Mn-SOD and catalase in T(4)-treated rats were differentially reduced by the administration of vitamin E and curcumin independently or in combination. Cu/Zn-SOD expression was ameliorated by both vitamin E and curcumin independently or in combination, whereas Mn-SOD expression was ameliorated by the supplementation of vitamin E or curcumin independently. However, the expression of catalase was alleviated by only supplementation of vitamin E to T(4)-treated rats. The results suggest that both vitamin E and curcumin may play an important role in protecting T(4)-induced oxidative stress in rat renal cortex by differentially modulating the activities of antioxidant enzymes and oxidative stress parameters.
Mol Biol Rep 2011 Feb
PMID:Regulation of expression of antioxidant enzymes by vitamin E and curcumin in L-thyroxine-induced oxidative stress in rat renal cortex. 2057 13


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