Logo - Rejuvenal
Vitamin E
Vitamin E; fat soluble vitamins
Introduction
The term vitamin E covers eight fat-soluble compounds found in nature. Four of them are called tocopherols and the other four tocotrienols. They are identified by the prefixes α, β, γ and δ. α-Tocopherol is the most common and biologically the most active of these naturally occurring forms of vitamin E. Natural tocopherols occur in RRR-configuration only (RRR-α-tocopherol was formerly designated as d-α-tocopherol). The chemical synthesis of α-tocopherol results in a mixture of eight different stereoisomeric forms which is called all-rac-α-tocopherol (or dl-α-tocopherol). The biological activity of the synthetic form is lower than that of the natural form.
The name tocopherol derives from the Greek words tocos, meaning childbirth, and pherein, meaning to bring forth. The name was coined to highlight its essential role in the reproduction of various animal species.
The ending -ol identifies the substance as being an alcohol.
The importance of vitamin E in humans was not accepted until fairly recently. Because its deficiency is not manifested by a well-recognised, widespread vitamin deficiency disease such as scurvy (vitamin C deficiency) or rickets (vitamin D deficiency), science only began to recognise the importance of vitamin E at a relatively late stage.
Functions
The major biological function of vitamin E is that of a lipid soluble antioxidant preventing the propagation of free-radical reactions. Free radicals are formed in normal metabolic processes and upon exposure to exogenous toxic agents (e.g. cigarette smoke, pollutants). Vitamin E is located within the cellular membranes. It protects polyunsaturated fatty acids (PUFAs) and other components of cellular membranes from oxidation by free radicals. Apart from maintaining the integrity of the cell membranes in the human body, it also protects low density lipoprotein (LDL) from oxidation.
Recently, non-antioxidant functions of α-tocopherol have been identified.
α-Tocopherol inhibits protein kinase C activity, which is involved in cell proliferation and differentiation. Vitamin E inhibits platelet aggregation and enhances vasodilation. Vitamin E enrichment of endothelial cells downregulates the expression of cell adhesion molecules, thereby decreasing the adhesion of blood cell components to the endothelium.
Rejuvenal ONLY uses natural vitamin E's in mixed form. We never use synthetic vitamin E.
Vitamin E and apoptosis
Sylvester PW. Vitam Horm. 2007;76:329-56.
College of Pharmacy, University of Louisiana at Monroe, Monroe, Louisiana 71209, USA.
Vitamin E is a generic term that refers to a family of compounds that is further divided into two subgroups called tocopherols and tocotrienols. All natural forms of tocopherols and tocotrienols are potent antioxidants that regulate peroxidation reactions and controls free radical production within the body. However, it is now firmly established that many of the biological actions mediated by individual vitamin E isoforms are not dependent on their antioxidant activity. Furthermore, synthetic ether derivatives of vitamin E that no longer possess antioxidant activity also display a wide range of biological activities. One of the most intriguing therapeutic applications for natural vitamin E and vitamin E derivatives currently being investigated is their use as anticancer agents. Specific forms of vitamin E display potent apoptotic activity against a wide range of cancer cell types, while having little or no effect on normal cell function or viability. Experimental studies have also determined that the intracellular mechanisms mediating the apoptotic effects of specific vitamin E compounds display great diversity in different types of caner cells and has been found to restore multidrug resistant tumor cells sensitivity to chemotherapeutic agents. These findings strongly suggest that some natural and synthetic analogues of vitamin E can be used effectively as anticancer therapy either alone or in combination to enhance the therapeutic efficacy and reduce toxicity of other anticancer agents.
PMID: 17628180 [PubMed - indexed for MEDLINE]
Antioxidants and cardioprotection
Applied Human Sciences, Department of Health and Exercise Science, Colorado State University, Fort Collins, CO.
Limiting myocardial ischemia-reperfusion (IR) injury is essential for preventing contractile dysfunction and limiting morbidity and mortality associated with ischemic heart disease. Over the last few decades, it has become clear that during IR insults, myocardial oxygen radical formation is accelerated and plays a critical role in mediating cellular damage and dysfunction. This review provides a brief summary of a variety of approaches that have been undertaken to alleviate the oxidant stress associated with myocardial IR, and a summary of the data demonstrating the potential therapeutic value of oxidant scavenging in limiting IR-induced myocardial damage. Included is a review of investigations using novel free radical scavengers, antioxidant extracts from a variety of plants, polyphenolic compounds from foods such as cocoa, soy, grapes, and wine, as well as vitamin E, vitamin C, and beta-carotene. Also reviewed is the evidence that exercise-induced increases in endogenous antioxidants may be an important change contributing to cardioprotection. One must conclude from this brief review that current evidence suggests that enhancing oxidant-scavenging capacity protects against some of the cardiomyocyte disturbances during IR and helps salvage myocardial tissue. Data in cultured cell and animal models are convincing; trials in humans are significantly more conflicting, but still promising.
The Selenium and Vitamin E Cancer Prevention Trial: rationale and design.
Klein EA, Thompson IM, Lippman SM, Goodman PJ, Albanes D, Taylor PR, Coltman C.
Section of Urologic Oncology, Department of Urology, Cleveland Clinic Foundation, Cleveland, Ohio, USA. Prostate Cancer Prostatic Dis. 2000 Nov;3(3):145-151.
Prostate cancer is the commonest non-skin malignancy in the United States and has a substantial mortality rate despite the use of PSA-based screening. Furthermore, therapy for prostate cancer by surgery, radiotherapy or hormonal manipulation carries a significant risk of treatment-related morbidity. Recent analysis of secondary endpoints of several large-scale randomized prospective clinical trials for other malignancies has suggested that selenium or vitamin E may result in a decreased incidence and mortality from prostate cancer. In vitro and preclinical studies of these antioxidants support this hypothesis. This review outlines the rationale and design of SELECT, the Selenium and Vitamin E Cancer Prevention Trial, designed to test the hypothesis that selenium or vitamin E alone or in combination can reduce the clinical incidence of prostate cancer in a population-based cohort of men at risk. SELECT is a phase III, randomized, double-blinded, prospective, 2x2 factorial clinical trial which will randomize 32,400 healthy men with normal DRE and serum PSA to one of four study arms: selenium alone, vitamin E alone, selenium+vitamin E, or placebo.
Study agents will be taken orally for a minimum of 7 and maximum of 12 y with assessments of general health, incident prostate cancer and toxicity performed at 12 month intervals. Under the assumptions described, the detectable risk reduction is 25% for an effective single agent relative to placebo, with an additional 25% reduction for the combination relative to an effective single agent. The estimated power for the comparison of a single agent vs placebo is 96% and the power for the comparison of an effective single agent vs combination is 89%. Secondary endpoints will include prostate cancer-free survival, all-cause mortality, and the incidence and mortality of other cancers and diseases potentially impacted by the chronic use of selenium and vitamin E. Other trial objectives will include periodic quality of life assessments, assessment of serum micronutrient levels and prostate cancer risk, and studies of the evaluation of biological and genetic markers with the risk of prostate cancer. Prostate Cancer and Prostatic Diseases (2000) 3, 145-151
Vitamin E Suppresses Enhancement of Factor VIII-Dependent Thrombin Generation by Systemic Hypoxia.
Wang JS, Cheng ML, Yen HC, Lou BS, Liu HC. Stroke. 2008 Oct 23.
From the Graduate Institute of Rehabilitation Science and Center for Healthy Aging Research, the Graduate Institute of Medical Biotechnology, and the General Education Center, Chang Gung University, Tao-Yuan, Taiwan.
BACKGROUND AND PURPOSE: Increased thrombin activity is an essential component of hemostatic reactions. This study elucidates how various hypoxic interventions impact endogenous thrombin generation (TG) after treatment with/without lipophilic antioxidant vitamin E.
METHODS: Twenty-four healthy sedentary men were randomly assigned to vitamin E (n=12) and placebo (n=12) groups. These subjects were randomly exposed to 12% (severe hypoxia), 15% (moderate hypoxia), 18% (light hypoxia), and 21% (normoxia) O2 for 2 hours in a normobaric hypoxia chamber. A novel calibrated, automated thrombinography approach was used to measure TG in plasma.
RESULTS: In the placebo group, severe hypoxia enhanced plasma FVIII level/activity and TG, which was accompanied by increased urinary 15-F2t-8-isoprostane level and decreased plasma total antioxidant content and superoxide dismutase activity. However, depletion of FVIII by incubation with anti-FVIII antibodies in plasma suppressed enhancement of TG by severe hypoxia. After administration of 1000 IU vitamin E, severe hypoxia did not significantly alter urinary 15-F2t-8-isoprostane level and plasma total antioxidant content, superoxide dismutase activity, FVIII level/activity, or TG. Moreover, redox status, FVIII level/activity, and TG were constant in response to moderate hypoxia, light hypoxia, and normoxia in the placebo and vitamin E groups.
CONCLUSIONS: We conclude that severe hypoxia promotes FVIII-dependent TG, likely by elevating oxidative stress; this hypoxic effect was ameliorated by pretreatment with vitamin E.
Vit E & Oxidative stress