Vitamin E (vitamin-e)

Healing Properties

  • Anticancer agent: Induces apoptosis (cell death) in various forms of cancer cells.
  • Antiinflammatory: Reduces inflammation.
  • Liver Health: A lower concentration of several biomarkers of inflammation in the liver have been observed in mice.[1]

Disease / Symptom Treatment

  • Colon Cancer: Has been shown to significantly suppress the growth and multiplicity of colon tumors.[2]
  • Lung Cancer: Vitamin E induces cell death in lung cancer cells by interrupting sphingolipid synthesis.[3]
  • Prostate Cancer: Vitamin E induces cell death in human prostate cancer cells by interrupting sphingolipid synthesis.[3]

Adverse Reactions

  • Vitamin E can not only work as an anti-oxidant but also as a pro-oxidant.[1]
  • Higher doses of vitamin E may cause tissue toxicity and an increased level of inflammation and oxidative stress in the kidney and liver.[1]
  • 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.[1]
  • Taking supplements with high doses of vitamin E is not recommended.[1]

Sources

  1. 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: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4964537/
    Citations:

  2. 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: http://doi.org/10.1016/j.freeradbiomed.2016.03.018
    Citations:

  3. 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: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC535585/
    Citations: