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Vitamin E

Vitamin E (vitamin-e) refers to a group of eight fat soluble organic compounds that include four tocopherols (alpha, beta, delta, gamma) and four tocotrienols (alpha, beta, delta, gamma).

Healing Properties

Antioxidant

Vitamin E is an exogenous antioxidant (exogenous antioxidants are antioxidants we get from our diet by eating antioxidant-rich foods and by taking supplements).[1]

Skin Health

Vitamin E has skin barrier-stabilizing properties.[2]

  • The skin barrier is the outermost layer of your skin's surface, and it consists of cells and lipids (fats). Also known as the permeability barrier, moisture barrier, or lipid barrier, the skin barrier is responsible for making sure essential water and electrolytes don't evaporate from skin.[3]

Photoprotective

Vitamin E has photoprotective effects.

  • Photoprotection is the biochemical process that helps organisms cope with molecular damage caused by sunlight.[2]
UV Light

UV-Light exposure has been shown to cause Vitamin E depletion in the body. Therefore Vitamin E supplementation before UV-Light exposure may be beneficial.[2]

Eicosanoid system

Vitamin E is known to produce anti-inflammatory effects by interacting with the signaling molecules produced by the eicosanoid system which may compliment the photoprotective effects of other antioxidants in the skin.[2]

  • The eicosanoid system involves the production of signaling molecules made by the oxidation of arachidonic acid or other polyunsaturated fatty acids.
    • These molecules function in diverse and important ways such as:
      • Mounting or inhibiting inflammation
      • Allergy Responses
      • Fever and other immune responses
      • Regulating the abortion of pregnancy and normal childbirth
      • Contributing to the perception of pain
      • Regulating cell growth
      • Controlling blood pressure
      • Modulating the regional flow of blood to tissues
    • Eicosanoid molecules most often act as autocrine signaling agents to impact their cells of origin or as paracrine signaling agents to impact cells in the proximity of their cells of origin. However, eicosanoids may also act as endocrine agents to control the function of distant cells.

Anticancer agent

Induces apoptosis (cell death) in various forms of cancer cells.

Antiinflammatory

Vitamin E Reduces inflammation.

  • Vitamin E is known to produce anti-inflammatory effects by interacting with the signaling molecules produced by the eicosanoid system.[2]

Liver Health

A lower concentration of several biomarkers of inflammation in the liver have been observed in mice.[4]

Disease / Symptom Treatment

Colon Cancer

Has been shown to significantly suppress the growth and multiplicity of colon tumors.[5]

Lung Cancer

Vitamin E induces cell death in lung cancer cells by interrupting sphingolipid synthesis.[6]

Prostate Cancer

Vitamin E induces cell death in human prostate cancer cells by interrupting sphingolipid synthesis.[6]

Adverse Reactions

Vitamin E can not only work as an anti-oxidant but also as a pro-oxidant.[4]

  • Higher doses of vitamin E may cause tissue toxicity and an increased level of inflammation and oxidative stress in the kidney and liver.[4]
  • The intake of high single doses of vitamin E can have detrimental effects, such as a higher risk for cardiovascular diseases and prostate cancer and even higher mortality.[4]
  • Taking supplements with high doses of vitamin E is not recommended.[4]

Sources:

  1. “Endogenous And Exogenous Antioxidants Benefits.” UKEssays.com, www.ukessays.com/essays/biology/using-endogenous-and-exogenous-antioxidants-biology-essay.php.

  2. Study Type: Preprint: Review Paper
    Title: An extensive Review of Sunscreen and Suntan Preparations
    Author(s): AK Mohiuddin
    Institution(s): Department of Pharmacy, World University of Bangladesh; 151/8, Green Road, Dhanmondi, Dhaka –1205, Bangladesh
    Publication: Preprint
    Date: April 2019
    Abstract: The sunscreen industry is achieving remarkable worldwide prominence by responding to the growing need for skin protection with fast-paced innovation. Increased consumer awareness of the harmful effects of sunlight has fueled the demand for improved photo protection. The need for broad-spectrum protection from both UVA and UVB rays has inspired scientists worldwide to research new cosmetic formulations and delivery systems. More effective sunscreen actives, emollients and novel cosmetic and functional ingredients have been regularly added to the formulator’s repertoire. Creativity in innovation has been hindered only by regulatory agencies and patent restrictions worldwide. Familiarity with the current restrictive regulations and patent law infringements has become integral to any research effort attempting to provide improved protection to individuals affected by the sun’s damaging effects. The increasing incidence of skin cancers and photo damaging effects caused by ultraviolet radiation has increased the use of sun screening agents, which have shown beneficial effects in reducing the symptoms and reoccurrence of these problems. Unlike the situation in Europe where sunscreen ingredients are considered under cosmetics guidelines, the FDA is required to define sunscreens as drugs since they are advertised to prevent sunburn and, more recently, the risk of skin cancer. In the USA, the FDA has been regulating this industry since August 25, 1978, with the publication of the Advance Notice of Proposed Rulemaking. Sunscreens are considered drugs and cosmetics and therefore must be governed by the FDA-OTC monograph. With the variety of sunscreen agents used in cosmetic and UV protection products, Australia, Canada, and the European Union (EU) have also developed regulatory protocols on safe sunscreen product use. Unlike the USA though, Australia has approved 34 active sunscreen ingredients and the EU has approved 28 of these ingredients. Current FDA regulations allow labeling of sunscreen products to a maximum of 30þ, despite the many products currently available with numbers as high as 100. From a cosmetic formulation point of view, increasing the SPF number in a product is governed by simple chemical principles.
    Link: Source
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  3. “Understanding Your Skin Barrier (and How to Keep It Healthy).” Beverly Hills MD, 6 Mar. 2019, beverlyhillsmd.com/understanding-skin-barrier/.

  4. Study Type: Animal Study
    Title: Tissue-Specific Effects of Vitamin E Supplementation
    Author(s): Eugene Jansen, Dale Viezeliene, Piet Beekhof, Eric Gremmer, and Leonid Ivanov
    Publication: International Journal of Molecular Sciences
    Date: 19 July 2016
    Abstract: A multivitamin and mineral supplementation study of 6 weeks was conducted with male and female mice. The control group received a standard dose of vitamins and minerals of 1x the Recommended Daily Intake (RDI), whereas a second group received 3x RDI. A third group received a high dose of vitamin E (25xRDI), close to the upper limit of toxicity (UL), but still recommended and considered to be harmless and beneficial. The high dose of vitamin E caused a number of beneficial, but also adverse effects. Different biomarkers of tissue toxicity, oxidative stress related processes and inflammation were determined. These biomarkers did not change in plasma and erythrocytes to a large extent. In the liver of male mice, some beneficial effects were observed by a lower concentration of several biomarkers of inflammation. However, in the kidney of male mice,a number of biomarkers increased substantially with the higher dose of vitamin E, indicating tissue toxicity and an increased level of inflammation. Since this dose of vitamin E, which is lower than theUL, cause some adverse effects, even after a short exposure period, further studies are required to reconsider the UL for vitamin E.Keywords:vitamin E;-tocopherol; oxidative stress; MCP-1; PAI-1; resistin; Il-6; TNF-1. IntroductionVitamins are generally considered beneficial for a number of physiological processes, such as anti-oxidant status. Also, the risk for several (chronic) diseases can be reduced by an adequate vitamin status. Consequently, including an efficient marketing strategy, supplementation of multi-vitamins is very popular in the general population. The anti-oxidant properties were partially attributed to vitamin E, a fat-soluble vitamin, which is a key component in the detoxification of oxidation processes, mainly in rodents. In particular, lipid peroxidation of polyunsaturated fatty acids can be inactivated by the presence of membrane-bound tocopherols. There have recently been a number of human studies, where the intake of high single doses of vitamin E can have detrimental effects, such as a higher risk for cardiovascular diseases and prostate cancer and even higher mortality. Taking supplements with high doses of vitamin E is not recommended, since vitaminE can not only work as an anti-oxidant but apparently also as a pro-oxidant.In this study, we have examined the effects of three-fold RDI of multi-vitamins and minerals in mice. In addition, a high dose of 25-fold RDI of vitamin E was used, which is still below the established level of toxicity. In both exposure studies, possible adverse effects of vitamin E on biomarkers of oxidative stress, redox status and liver and kidney were monitored in the circulation (plasma and erythrocytes) and in liver and kidney tissue.
    Link: Source
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  5. Study Type: Animal Study
    Title: Vitamin E metabolite 13′-carboxychromanols inhibit pro-inflammatoryenzymes, induce apoptosis and autophagy in human cancer cells bymodulating sphingolipids and suppress colon tumor development inmice
    Author(s): Yumi Jang, Na-Young Park, Agnetha Linn Rostgaard-Hansen, Jianjie Huang, Qing Jiang
    Institution(s): Department of Nutrition Science, Purdue University, West Lafayette, IN 47907, USA
    Publication: Free Radical Biology and Medicine
    Date: 23 March 2016
    Abstract: Vitamin E forms are substantially metabolized to various carboxychromanols including 13′-carbox-ychromanols (13′-COOHs) that are found at high levels in feces. However, there is limited knowledgeabout functions of these metabolites. Here we studiedδT-13′-COOH andδTE-13′-COOH, which aremetabolites ofδ-tocopherol andδ-tocotrienol, respectively.δTE-13′-COOH is also a natural constituent ofa traditional medicineGarcinia Kola.Both13′-COOHs are much stronger than tocopherols in inhibition ofpro-inflammatory and cancer promoting cyclooxygenase-2 (COX-2) and 5-lipoxygenase (5-LOX), and ininduction of apoptosis and autophagy in colon cancer cells. The anticancer effects by 13′-COOHs ap-peared to be partially independent of inhibition of COX-2/5-LOX. Using liquid chromatography tandemmass spectrometry, we found that 13′-COOHs increased intracellular dihydrosphingosine and dihy-droceramides after short-time incubation in HCT-116 cells, and enhanced ceramides while decreasedsphingomyelins during prolonged treatment. Modulation of sphingolipids by 13′-COOHs was observedprior to or coinciding with biochemical manifestation of cell death. Pharmaceutically blocking the in-crease of these sphingolipids partially counteracted 13′-COOH-induced cell death. Further, 13′-COOHinhibited dihydroceramide desaturase without affecting the protein expression. In agreement with thesemechanisticfindings,δTE-13′-COOH significantly suppressed the growth and multiplicity of colon tumorin mice. Our study demonstrates that 13′-COOHs have Antiinflammatory and anticancer activities, maycontribute toin vivoanticancer effect of vitamin E forms and are promising novel cancer preventionagents.
    Link: Source
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  6. Study Type: Human Study: In Vitro
    Title: γ-Tocopherol or combinations of vitamin E forms induce cell death in human prostate cancer cells by interrupting sphingolipid synthesis
    Author(s): Qing Jiang, Jeffrey Wong, Henrik Fyrst, Julie D. Saba, Bruce N. Ames
    Publication: National Academy of Sciences: Proceedings of the National Academy of Sciences of the United States of America
    Date: 2004 Dec 21
    Abstract: γ-Tocopherol (γT), the predominant form of vitamin E in diets, but not α-tocopherol, the major vitamin E form in tissues and supplements, inhibits proliferation of prostate cancer cells (LNCaP and PC-3) and lung cancer cells (A549). In contrast, at similar concentrations, γT has no effect on normal prostate epithelial cells. Combinations of some vitamin E forms, such as γT and δ-tocopherol, exhibit additive or synergistic inhibitory effects. In this study, γT or its combination with δ-tocopherol induced apoptosis in androgen-sensitive prostate LNCaP, but not in androgen-resistant PC-3 cells, by the induction of cytochrome c release, activation of caspase 9 and caspase 3, cleavage of poly-ADP-ribose polymerase (PARP), and involvement of caspase-independent pathways. Myriocin and fumonisin B1, specific inhibitors of key enzymes (serine palmitoyltransferase and dihydroceramide synthase, respectively) in de novo synthesis of sphingolipids, significantly protected cells from γT-induced DNA fragmentation, cytochrome c release, PARP cleavage, and the formation of active caspase 3. Compared with vehicle-treated controls, γT treatment led to pronounced dihydroceramide and dihydrosphingosine accumulation, which preceded morphological and biochemical manifestations of apoptosis. In contrast, ceramide and shpingosine levels did not increase until day 3, when substantial cell death took place. Our study demonstrates that γT and mixed vitamin E forms induce cell death by interrupting the de novo sphingolipid pathway in a prostate cancer cell line. Thus, certain vitamin E forms may be valuable as anticancer agents.
    Link: Source
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