E vitamin scientific update |
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Mol Aspects Med. 2007 Feb 23;
Neuzil J, Dong LF, Ramanathapuram L, Hahn T, Chladova M, Wang XF, Zobalova R, Prochazka L, Gold M, Freeman R, Turanek J, Akporiaye ET, Dyason JC, Ralph SJ.
Apoptosis Research Group, School of Medical Science, Griffith University, Southport, Qld, Australia; Molecular Therapy Group, Institute of Molecular Genetics, Czech Academy of Sciences, Prague, Czech Republic.
Vitamin E analogues as a novel group of mitocans: Anti-cancer agents that act by targeting mitochondria.
Mitochondria have recently emerged as new and promising targets for cancer prevention and therapy. One of the reasons for this is that mitochondria are
instrumental to many types of cell death and often lie downstream from the initial actions of anti-cancer drugs. Unlike the tumour suppressor gene encoding
p53 that is notoriously prone to inactivating mutations but whose function is essential for induction of apoptosis by DNA-targeting agents (such as
doxorubicin or 5-fluorouracil), mitochondria present targets that are not so compromised by genetic mutation and whose targeting overcomes problems with
mutations of upstream targets such as p53. We have recently proposed a novel class of anti-cancer agents, mitocans that exert their anti-cancer activity by
destabilising mitochondria, promoting the selective induction of apoptotic death in tumour cells. In this communication, we review recent findings on
mitocans and propose a common basis for their mode of action in inducing apoptosis of cancer cells. We use as an example the analogues of vitamin E that are
proving to be cancer cell-specific and may soon be developed into efficient anti-cancer drugs.
J Trace Elem Med Biol. 2007;21(2):113-9.
Faure P, Barclay D, Joyeux-Faure M, Halimi S.
Laboratoire HP2, Hypoxie Physio-Pathologie Respiratoire et Cardiovasculaire, Inserm ERI 0017, Faculte de Medecine-Pharmacie, BP 217, 38043 Grenoble cedex 9, France.
Comparison of the effects of zinc alone and zinc associated with selenium and vitamin E on insulin sensitivity and oxidative stress in high-fructose-fed rats.
PURPOSE: In the present study, we investigated the effect of an association of micronutrients (zinc (Zn), selenium (Se) and vitamin E (vit E)) on insulin
activity and antioxidant status in an animal model of insulin resistance, the high-fructose-fed rat. PROCEDURES: Five experimental groups were compared: a
control group (C) receiving a standard diet, a high-fructose-fed group (F) where 58% of the diet carbohydrate was fructose, a high-fructose-fed group
supplemented with Zn alone (FZn group), a high-fructose-fed group supplemented micronutrients (Zn, Se and vit E) (FMicro group). A fifth group consumed a
high-fructose diet and received metformin in the drinking water (200mg/day/rat) (FMet group). Insulin sensitivity was measured using the euglycemic
hyperinsulinic glucose clamp technique. Metabolic parameters, trace elements and antioxidant parameters were measured in blood samples from all groups.
RESULTS: High-fructose-fed rats were resistant to insulin as indicated by the lower glucose infusion rate. The insulin sensitivity of FZn, FMicro and FMet
groups was higher than that of F group, with the highest insulin sensitivity for the FMicro group. No statistically significant difference in glycemia
between the groups was observed. The ratio of reduced to oxidized glutathione was higher in FZn and FMicro groups than in all other groups, as a consequence
of decreased oxidized glutathione. CONCLUSION: Our results provide direct evidence that micronutrients have a beneficial effect on insulin sensitivity and
some components of the antioxidant defense system in an animal model of insulin resistance.
Fertil Steril. 2007 May 4;
Aybek H, Aybek Z, Rota S, Sen N, Akbulut M.
Department of Biochemistry.
The effects of diabetes mellitus, age, and vitamin E on testicular oxidative stress.
OBJECTIVE: To examine the effects of age and/or diabetes on oxidative stress and steroidogenesis, and the protective effect of vitamin E in testis tissue.
DESIGN: Controlled experimental study. SETTING: Pamukkale University School of Medicine animal facility. ANIMAL(S): Male Wistar rats divided into six groups
with six animals in each group: young control; young diabetic; young diabetic with vitamin E treatment; aged control; aged diabetic; and aged diabetic with
vitamin E treatment. INTERVENTION(S): Diabetes was induced by a single intraperitoneal injection of 50 mg/kg streptozotocin and was confirmed by testing
blood glucose levels 5 to 7 days after injection. Vitamin E was administered orally for 6 weeks. MAIN OUTCOME MEASURE(S): Serum testosterone and tissue
malondialdehyde (MDA), superoxide dismutase (SOD), glutathione (GSH) levels were measured, and testis tissue was examined histopathologically. RESULT(S):
Elevated malondialdehyde and reduced superoxide dismutase, glutathione, and serum testosterone levels were detected only in the young and aged-diabetic
groups. Histopathologic change was not detected in the testis tissue in any of the groups. CONCLUSION(S): Age does not alter the effects of diabetes-induced
free radical damage in testis tissue; improvement in this damage can be achieved by vitamin E treatment.
Clin Exp Hypertens. 2007 Mar-Apr;29(3):135-48.
Fardoun RZ.
Heart and Kidney Institute, University of Houston, College of Pharmacy. Houston, Texas. USA.
The use of vitamin e in type 2 diabetes mellitus.
Diabetes mellitus has assumed epidemic proportions in most parts of the world, and it is a major source of morbidity in developed countries. In addition, in
several instances, diabetes is associated with a variety of metabolic abnormalities, including abdominal obesity, insulin resistance, hypertension,
dyslipidemia, and hyperglycemia. There is considerable evidence that hyperglycemia causes the generation of reactive oxygen species (ROS), ultimately leading
to increased oxidative stress in a variety of tissues. In the absence of an appropriate compensatory response by the endogenous antioxidants, such as
vitamins C and E, catalase, glutathione, and superoxide dismutase, oxidative stress dominates, resulting in the activation of stress-sensitive intracellular
signaling pathways. One of the major consequences is the generation of gene products that cause cellular damage and are ultimately responsible for the late
complications of diabetes. The ability of antioxidants to protect against the effects of hyperglycemia in vitro, along with the clinical benefits often
reported following antioxidant therapy, supports a causative role of oxidative stress in mediating and/or worsening these abnormalities. This review will
focus on the critical assessment of the literature as it relates to the association between oxidative stress and diabetes, followed by the role of oxidative
stress in the complications of type 2 diabetes mellitus. Finally, a review of the use of the antioxidant vitamin E will be provided in diabetic patients by
assessing and evaluating some of the clinical trials in the literature.
Surgery. 2006 Oct;140(4):607-15.
Peralta EA, Viegas ML, Louis S, Engle DL, Dunnington GL.
Department of Surgery, Southern Illinois University School of Medicine, Springfield, Ill.
Effect of vitamin E on tamoxifen-treated breast cancer cells.
BACKGROUND: Induction of apoptosis by tamoxifen has been postulated to involve oxidative stress. Tamoxifen (TAM) may act on estrogen receptors (ER) located in the plasma membrane. Our hypothesis that supplemental antioxidant vitamin E (alpha-tocopherol) acts at the plasma membrane to alter the effectiveness of tamoxifen was tested in ER-positive breast cancer cell lines, MCF-7 and T47D. METHODS: Cells were treated in vitro with 20-muM TAM alone and in combination with 10-muM alpha-tocopherol (AT). Estrogen growth signals were quantified by immunohistochemical staining for the mitogen-activated protein kinase p-ERK. Rapid changes in intracellular calcium were detected in TAM-treated MCF-7 and T-47D cells by fluorescence microscopy of cells loaded with the calcium-sensitive dye Fluo 4AM. Apoptosis was assayed by flow cytometry. RESULTS: Proliferating cells in normal medium exhibited strong p-ERK staining. Addition of TAM abolished p-ERK staining and caused cell rounding and death. The addition of AT led to the restoration of cell proliferation and p-ERK expression even in the presence of high-dose TAM. Intracellular calcium rapidly increased in MCF-7 and T47D cells upon exposure to TAM, followed by an increase in caspase activation and eventual apoptosis. The increase in intracellular calcium was abolished by the addition of 10muM AT to TAM, and pan-caspase staining decreased at 5 hours from 72% to 41%. CONCLUSIONS: These studies suggest that supplemental vitamin E decreases the inhibitory effect of TAM on the proliferation of ER+ breast cancer cells and eliminates the rapid rise in intracellular calcium that leads to apoptosis stimulated by TAM. The use of vitamin E acetate supplements may be inadvisable for women taking tamoxifen.
Bundesgesundheitsblatt Gesundheitsforschung Gesundheitsschutz. 2006 Oct 4;
Siekmeier R, Steffen C, Marz W.
Bundesinstitut fur Arzneimittel und Medizinprodukte (BfArM), Bonn, BRD.
[Can antioxidants prevent atherosclerosis?][Article in German]
In vitro studies have shown that antioxidants (e. g. beta-carotene, vitamin C and vitamin E) can interfere with some pathomechanisms of atherosclerosis and therefore might have a protective effect. From the investigated antioxidants vitamin E showed the best effect. Some animal and epidemiological studies confirmed such a protective effect in vivo especially after administration of high doses of vitamin E. However, most of the placebo-controlled studies for primary or secondary prevention failed to show a protective effect even after administration of high doses. In addition, other studies demonstrated a risk for adverse effects due to antioxidant supplementation (beta-carotene and vitamin E). Our review summarises the principle of antioxidant supplementation and a number of relevant epidemiological and clinical studies for prevention of atherosclerosis. The obtained results suggest that supplementation of antioxidants cannot be recommended for the normal population.
E vitamin description...
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Drug category:Antioxidants and Vitamines
 E vitamin scientific update
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