비타민E (알파토코페롤)

BACKGROUND: Recently, it has been discovered that anti-inflammatory and anti-oxidative pathways play a role in depression and anxiety. Lower serum levels of antioxidants, such as vitamin E, have been implicated in both depression and anxiety. METHODS: This PROSPERO-registered systematic review (Reference: CRD42021260058) is reported according to PRISMA guidelines. PubMed, EMBASE, CENTRAL, PsycINFO, and CINAHL were searched from inception to June 2021. RESULTS: Twelve studies were included in this systematic review, and nine in meta-analysis of vitamin E versus placebo. For depression, meta-analysis of 354 participants showed a standardised mean difference of -0.88 (95% CI: -1.54, -0.21; I2 = 87%) favouring vitamin E. For anxiety, meta-analysis of 306 participants showed a standardised mean difference of -0.86 (95% CI: -2.11, 0.40; I2 = 95%) favouring vitamin E. Three of the studies involved a pure comparison of vitamin E against placebo, while others included constituents such as omega-3 fatty acids. Nine of the studies were at low risk of bias, two had some concerns, and one was at high risk of bias. CONCLUSION: Vitamin E supplementation has shown inconclusive results in ameliorating both depression and anxiety. Containing a reassuring safety profile and low cost, future studies would be of promise, and they would benefit from both larger sample sizes and from excluding other constituents, such as omega-3 fatty acids, from experimental and comparator arms.

BACKGROUND AND AIMS: The studies have shown that α-tocopherol supplementation could improve lipid profile in diabetes mellitus (DM) patients. Nonetheless, the result remains inconsistent. Therefore, this meta-analysis was performed to evaluate the efficacy of α-tocopherol supplement on lipid parameters in DM patients. METHODS: We conducted an extensive search via Cochrane Library, PubMed, Scopus, and Web of Science databases to acquire the reported RCTs up to October 2020. RESULTS: The results showed no effects of α-tocopherol supplementation on lipid profile in DM patients except when used ≥12 weeks. CONCLUSIONS: α-tocopherol supplementation in DM patients had no significant effect on lipid profiles.

The previous meta-analysis of clinical trials revealed a beneficial effect of vitamin E supplementation on serum C-reactive protein (CRP) concentrations; however, it is unknown whether this vitamin has the same influence on other inflammatory biomarkers. Also, several clinical trials have been published since the release of earlier meta-analysis. Therefore, we aimed to conduct a comprehensive meta-analysis to summarize current evidence on the effects of vitamin E supplementation on inflammatory biomarkers in adults. We searched the online databases using relevant keywords up to November 2019. Randomized clinical trials (RCTs) investigating the effect of vitamin E, compared with the placebo, on serum concentrations of inflammatory cytokines were included. Overall, we included 33 trials with a total sample size of 2102 individuals, aged from 20 to 70 years. Based on 36 effect sizes from 26 RCTs on serum concentrations of CRP, we found a significant reduction following supplementation with vitamin E (- 0.52, 95% CI - 0.80, - 0.23 mg/L, P < 0.001). Although the overall effect of vitamin E supplementation on serum concentrations of interleukin-6 (IL-6) was not significant, a significant reduction in this cytokine was seen in studies that used α-tocopherol and those trials that included patients with disorders related to insulin resistance. Moreover, we found a significant reducing effect of vitamin E supplementation on tumor necrosis factor-α (TNF-α) concentrations at high dosages of vitamin E; such that based on dose-response analysis, serum TNF-α concentrations were reduced significantly at the dosages of ≥ 700 mg/day vitamin E (Pnon-linearity = 0.001). Considering different chemical forms of vitamin E, α-tocopherol, unlike other forms, had a reducing effect on serum levels of CRP and IL-6. In conclusion, our findings revealed a beneficial effect of vitamin E supplementation, particularly in the form of α-tocopherol, on subclinical inflammation in adults. Future high-quality RCTs should be conducted to translate this anti-inflammatory effect of vitamin E to the clinical setting.

BACKGROUND: Vitamin E occurs naturally in the diet. It has several biological activities, including functioning as an antioxidant to scavenge toxic free radicals. Evidence that free radicals may contribute to the pathological processes behind cognitive impairment has led to interest in the use of vitamin E supplements to treat mild cognitive impairment (MCI) and Alzheimer's disease (AD). This is an update of a Cochrane Review first published in 2000, and previously updated in 2006 and 2012. OBJECTIVES: To assess the efficacy of vitamin E in the treatment of MCI and dementia due to AD. SEARCH METHODS: We searched the Specialized Register of the Cochrane Dementia and Cognitive Improvement Group (ALOIS), the Cochrane Library, MEDLINE, Embase, PsycINFO, CINAHL, LILACS as well as many trials databases and grey literature sources on 22 April 2016 using the terms: "Vitamin E", vitamin-E, alpha-tocopherol. SELECTION CRITERIA: We included all double-blind, randomised trials in which treatment with any dose of vitamin E was compared with placebo in people with AD or MCI. DATA COLLECTION AND ANALYSIS: We used standard methodological procedures according to the Cochrane Handbook for Systematic Reviews of Interventions. We rated the quality of the evidence using the GRADE approach. Where appropriate we attempted to contact authors to obtain missing information. MAIN RESULTS: Four trials met the inclusion criteria, but we could only extract outcome data in accordance with our protocol from two trials, one in an AD population (n = 304) and one in an MCI population (n = 516). Both trials had an overall low to unclear risk of bias. It was not possible to pool data across studies owing to a lack of comparable outcome measures.In people with AD, we found no evidence of any clinically important effect of vitamin E on cognition, measured with change from baseline in the Alzheimer's Disease Assessment Scale - Cognitive subscale (ADAS-Cog) over six to 48 months (mean difference (MD) -1.81, 95% confidence interval (CI) -3.75 to 0.13, P = 0.07, 1 study, n = 272; moderate quality evidence). There was no evidence of a difference between vitamin E and placebo groups in the risk of experien

The current analysis reexamines the relationship between supplemental vitamin E and all-cause mortality. All randomized, controlled trials testing the treatment effect of vitamin E supplementation in adults for at least one year were sought. MEDLINE, the Cochrane Library, and Biological Abstracts databases were searched using the terms "vitamin E," "alpha-tocopherol," "antioxidants," "clinical trial," and "controlled trial" for studies published through April 2010; results were limited to English, German, or Spanish language articles. Studies were also obtained through reference mining. All randomized controlled trials using vitamin E, with a supplementation period of at least one year, to prevent or treat disease in adults were identified and abstracted independently by two raters. Mortality data from trials with a supplementation period of at least one year were pooled. The selected trials (n = 57) were published between 1988 and 2009. Sample sizes range from 28 to 39,876 (median = 423), yielding 246,371 subjects and 29,295 all-cause deaths. Duration of supplementation for the 57 trials range from one to 10.1 years (median = 2.6 years). A random effects meta-analysis produce an overall risk ratio of 1.00 (95% confidence interval: 0.98, 1.02); additional analyses suggest no relationship between dose and risk of mortality. Based on the present meta-analysis, supplementation with vitamin E appears to have no effect on all-cause mortality at doses up to 5,500 IU/d.

A meta-analysis was performed to consolidate the results of studies which have evaluated the effects of Vitamin E supplementation during the dry period on the risk of retained foetal membranes (RFM) in the dairy cow. Twenty studies demonstrated a beneficial response to Vitamin E whilst 21 found no benefit and 3 reported an increase in the incidence of RFM in treated cows. The odds ratios (OR) of the available studies exhibited significant heterogeneity, so multivariable logistic regression analysis was performed to enable the identification of factors associated with the response to Vitamin E supplementation. Our multivariable analysis included parity and Vitamin E supplementation (control/treated) in the model, because all other factors were co-linear. Results indicated that Vitamin E supplementation led to a reduction in the incidence of RFM. A second multivariable analysis was undertaken on a subset of the data including only supplemented cows to determine the influence of supplementation factors on the risk of RFM. All factors were co-linear with each other, therefore, only type of Vitamin E supplementation was included in this analysis. The regression model demonstrated that administration of the synthetic Vitamin E alpha-tocopheryl acetate was associated with a lower risk of RFM than treatment with natural Vitamin E (alpha-tocopherol) (P=0.047, OR=0.49), whereas the difference between the synthetic Vitamin E alpha-tocopherol acetate and natural Vitamin E just failed to attain statistical significance (P=0.059, OR=0.53). Overall the analyses indicate that Vitamin E supplementation during the dry period is associated with a reduced risk of RFM, and that the synthetic forms of Vitamin E are more effective than the natural compound.

BACKGROUND: Vitamin E (α-tocopherol) is an essential micronutrient for human health and optimal physiological function. Inadequacy may be common due to a lack of bioavailability. The use of dietary lipids alongside other emulsification agents may elicit more robust serum concentrations of α-tocopherol via improved bioavailability. Therefore, the aim of the study was to examine oral bioavailability of two delivery methods of α-tocopherol, (1) a microemulsion gel formula composed of dietary lipids and other emulsification agents and (2) a dry solid tablet over 12 hours. METHODS: Twelve participants (age = 37.3 ± 9.6 years; height = 173.4 ± 11.8 cm; body mass = 71.2 ± 10.0 kg) participated in a double-blind, randomized, crossover trial comparing two delivery methods both dosed at 288 mg of α-tocopherol. Serum α-tocopherol concentrations were assessed from blood donated by participants at pre-consumption, 2-, 4-, 8-, and 12-hour post-consumption. Study conditions were separated by a 7-day washout. RESULTS: The microemulsion gel formula delivery demonstrated significantly greater area under the curve (p < 0.001) and serum concentration maximums (p = 0.003) for serum α-tocopherol compared to the tablet delivery. No significant differences were detected between conditions for the time to reach concentration maximums (p = 0.375). CONCLUSION: We conclude that a mixture of dietary lipids and emulsification agents in the form of a microemulsion gel formula was able to significantly improve bioavailability of serum α-tocopherol compared to a tablet by yielding higher serum α-tocopherol maximum concentrations and area under the curve over a 12-hour study period despite dosage being matched.

PURPOSE: The understanding of the role of plasma antioxidant levels in male fertility in the USA is limited. In a secondary analysis of the Males, Antioxidants, and Infertility (MOXI) randomized clinical trial, we sought to determine whether serum levels of vitamin E (α-tocopherol), zinc, and selenium were correlated with semen parameters and couple fertility outcomes. METHODS: This study is a secondary analysis of the MOXI clinical trial. The primary endpoints in this secondary analysis include semen parameters, and DNA fragmentation and clinical outcomes including pregnancy and live birth. Analyses were completed using Wilcoxon's rank-sum test and linear regression models. RESULTS: At baseline, the analysis included plasma labs for vitamin E (n = 131), selenium (n = 124), and zinc (n = 128). All baseline plasma values were in the normal ranges. There was no association between selenium, zinc, or vitamin E levels and semen parameters or DNA fragmentation. Baseline antioxidant levels in the male partners did not predict pregnancy or live birth among all couples. Among those randomized to placebo, baseline male antioxidant levels did not differ between those couples with live birth and those that did not conceive or have a live birth. CONCLUSIONS: Among men attending fertility centers in the USA, who have sufficient plasma antioxidant levels of zinc, selenium, or vitamin E, no association was observed between vitamins and semen parameters or clinical outcomes in couples with male infertility. Higher levels of antioxidants among men with circulating antioxidants in the normal range do not appear to confer benefit on semen parameters or male fertility. © 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.

INTRODUCTION: Nephrotoxicity remains a major long-standing concern for colistin, and it is critical to find agents that can prevent it. The present study aims to investigate the effect of vitamin E on the prevention of colistin-induced nephrotoxicity based on its antioxidant and free radical scavenging properties. METHODS: A randomized clinical trial was designed for 52 patients taking colistin. These patients were categorized into two groups of equal size, receiving colistin or colistin plus vitamin E (α-Tocopherol). Vitamin E with doses of 400 units was administrated daily either orally or by a nasogastric tube if needed. The incidence of Acute Kidney Injury (AKI) and its duration was recorded based on RIFLE criteria. RESULTS: The Incidence of AKI based on RIFLE criteria was 42.3% and 46.2% in intervention and control groups, respectively. The analysis showed no significant difference in the prevalence of AKI for the two groups (P = 0.78). There was no significant difference in the duration of AKI neither (P = 0.83). CONCLUSION: Although vitamin E is a powerful biological antioxidant, the effects of Vitamin E prophylaxis on colistin-induced nephrotoxicity was not taken into consideration in this study.

The precise understanding of the behaviour of vitamin E (α-tocopherol; Toc) complexed with cyclodextrin (CD) additives in aqueous solution is a fundamental issue for further development of their aqua-related biological applications. In this study, the solubilisation and complexation behaviours of Toc with methyl-substituted CD derivatives and the radical scavenging ability of the resulting complexes were precisely investigated in water media. Several problems were encountered upon pre-dissolving Toc in an organic solvent prior to the addition to the water media, such as enhancement of the dispersibility and decrease in the complexation capacity. Additionally, dispersions were obtained in some cases when mixing CD and Toc even in the absence of an organic solvent; therefore, to perform the measurements, a transparent solution was prepared via filtration with a nanopore filter. Consequently, unexpectedly, the addition of certain CD methylated derivatives did not always enhance the solubility of Toc significantly. However, 2,6-di-O-methylated β-CD (2,6-DMCD) formed a water-soluble inclusion complex with Toc, effectively enhancing its solubility. A phase solubility study indicated the formation of 1:2 or 1:3 Toc/CD inclusion complexes, and the interaction of 2,6-DMCD with both the chromanol head and the phytol chain of Toc was revealed by 2D ROESY nuclear magnetic resonance analysis. The interaction between 2,6-DMCD and the chromanol head was also confirmed for a 2,6-DMCD-2,2,5,7,8-pentamethyl-6-chromanol inclusion complex. Additionally, a rapid scavenging effect for molecularly dissolved Toc was demonstrated even in a system comprising a chromanol head directly encapsulated by CD. Hence, this work elucidated the precise complexation and radical scavenging ability of 2,6-DMCD-Toc in an aqueous solution, which paves the way for its biological applications.

Astaxanthin (Asx) is known to be a potent quencher of singlet oxygen and an efficient scavenger of superoxide anion. However, the scavenging activity of Asx toward the hydroxyl radical was currently unclear because the high lipophilicity of Asx prevents analysis of such activity in water. Liposomes containing Asx (Asx-lipo) were previously shown to be dispersed in water. Analysis of the hydroxyl radical scavenging activity of Asx-lipo demonstrated a dose-dependence in water, with the effect of Asx being more potent than the vitamin E α-tocopherol (α-T). Furthermore, liposomes co-encapsulating Asx and vitamin E derivatives, namely tocotrienols (T3), showed a synergistic elimination effect on singlet oxygen and hydroxyl radical, although the antioxidative activity of liposomes co-encapsulating Asx and α-T was lower than the calculated additive value of each independent activity. A calculation of the most stable structure of Asx in the presence of α-T or T3, suggested that only T3 was able to hydrogen bond with Asx, and the Asx polyene chain partially interacting with the α-T3 triene chain, which could explain the synergistic effect between Asx and T3, but not Asx and α-T. This review introduces the hydroxyl radical scavenging activity of Asx, and its synergistic effect with T3.

Inhibition of MAP kinase pathways by selective BRAF inhibitors, such as vemurafenib and dabrafenib, have evolved as key therapies of BRAF-mutated melanoma. However, tumor relapse and therapy resistance have remained as major problems, which may be addressed by combination with other pathway inhibitors. Here we identified the potassium channel inhibitor TRAM-34 as highly effective in combination with vemurafenib. Thus apoptosis was significantly enhanced and cell viability was decreased. The combination vemurafenib/TRAM-34 was also effective in vemurafenib-resistant cells, suggesting that acquired resistance may be overcome. Vemurafenib decreased ERK phosphorylation, suppressed antiapoptotic Mcl-1 and enhanced proapoptotic Puma and Bim. The combination resulted in enhancement of proapoptotic pathways as caspase-3 and loss of mitochondrial membrane potential. Indicating a special mechanism of vemurafenib-induced apoptosis, we found strong enhancement of intracellular ROS levels already at 1 h of treatment. The critical role of ROS was demonstrated by the antioxidant vitamin E (α-tocopherol), which decreased intracellular ROS as well as apoptosis. Also caspase activation and loss of mitochondrial membrane potential were suppressed, proving ROS as an upstream effect. Thus ROS represents an initial and independent apoptosis pathway in melanoma cells that is of particular importance for vemurafenib and its combination with TRAM-34.

Amphotericin B (AmB) remains the antifungal polyene of choice in deep fungal infections, but its high toxicity to mammalian cells limits its use. This toxicity is partly due to lipid peroxidation exerted by amphotericin B in cell membranes. The work we have undertaken focused on the one part the evaluation of the efficacy of amphotericin B in the presence of some antioxidants vitamins (vitamin C "ascorbic acid" and vitamin E "α-tocopherol") against the yeast Candida albicans ATCC 10231. Secondly, we have tested the cytotoxicity of these formulations on human red blood cells. The results showed a significant improvement in the efficiency of our formulations tested from 7% to 12% compared with amphotericin B alone at therapeutic concentrations. Furthermore, the addition of vitamin C and vitamin E protects human red blood cells against the cytotoxicity induced by amphotericin B with 17%. This is due may be to the antioxidant power of vitamins which confer protection against the autoxidation of the molecule of amphotericin B. On the other hand, it is noticed that the yeast regrows after 24h whatever in complex with vitamin C or vitamin E of the stock solution. On completion of this study, the incorporation of antioxidant vitamins that we propose to the reaction medium of antifungal improved the therapeutic index of amphotericin B.

Previous experiments in rats with chemically induced colitis have shown that the antioxidant N-acetylcysteine plus mesalamine (5-ASA) exerted a significantly greater therapeutic effect in promoting mucosal healing when compared to either agent alone. The aims of the present study were to compare the effects of three antioxidants plus mesalamine vs. 5-ASA alone in treatment of colitis induced by trinitrobenzene sulfonic acid (TNBS) in rats. METHODS: Three days following induction of TNBS colitis, rats received 8 days of rectal therapy with 5-ASA, or 5-ASA plus vitamin C (ascorbic acid), 5-ASA plus phenyl butylnitrone (PBN) and 5-ASA plus vitamin E (alpha-tocopherol). Distal colonic tissues were examined for microscopic colitis and myeloperoxidase (MPO) activity. RESULTS: Global assessments of microscopic colitis induced by TNBS indicated that 5-ASA alone significantly changed colonic injury by -31%. Combination therapy with ascorbic acid plus 5-ASA or alpha-tocopherol plus 5-ASA caused further significant change in TNBS colitis by -65 and -82%, respectively. Each of these values was significantly below scores observed with 5-ASA as monotherapy. Reduction in colitis with PBN plus 5-ASA was not different from 5-ASA alone. MPO activity was decreased significantly in response to monotherapy with 5-ASA and each of the antioxidants plus 5-ASA when compared to TNBS. alpha-Tocopherol plus 5-ASA, however, was the only treatment strategy that reduced significantly MPO activity below that recorded for 5-ASA alone. In conclusion, our results indicate that antioxidants other than N-acetylcysteine significantly enhance the therapeutic effectiveness of 5-ASA in the treatment of TNBS colitis. alpha-Tocopherol plus 5-ASA exerted profound anti-inflammatory and reparative effects upon colitis induced by TNBS.

Intense seizure activity associated with status epilepticus and excitatory amino acid (EAA) imbalance initiates oxidative damage and neuronal injury in CA1 of the ventral hippocampus. We tested the hypothesis that dendritic degeneration of pyramidal neurons in the CA1 hippocampal area resulting from seizure-induced neurotoxicity is modulated by cerebral oxidative damage. Kainic acid (KA, 1 nmol/5 microl) was injected intracerebroventricularly to C57Bl/6 mice. F2-isoprostanes (F2-IsoPs) and F4-neuroprostanes (F4-NeuroPs) were used as surrogate measures of in vivo oxidative stress and biomarkers of lipid peroxidation. Nitric oxide synthase (NOS) activity was quantified by evaluating citrulline level and pyramidal neuron dendrites and spines were evaluated using rapid Golgi stains and a Neurolucida system. KA produced severe seizures in mice immediately after its administration and a significant (p<0.001) increase in F2-IsoPs, F4-NeuroPs and citrulline levels were seen 30 min following treatment. At the same time, hippocampal pyramidal neurons showed significant (p<0.001) reduction in dendritic length and spine density. In contrast, no significant change in neuronal dendrite and spine density or F2-IsoP, F4-NeuroPs and citrulline levels were found in mice pretreated with vitamin E (alpha-tocopherol, 100mg/kg, i.p.) for 3 days, or with N-tert-butyl-alpha-phenylnitrone (PBN, 200mg/kg, i.p.) or ibuprofen (inhibitors of cyclooxygenase, COX, 14 microg/ml of drinking water) for 2 weeks prior to KA treatment. These findings indicate novel interactions among free radical-induced generation of F2-IsoPs and F4-NeuroPs, nitric oxide and dendritic degeneration, closely associate oxidative damage to neuronal membranes with degeneration of the dendritic system, and point to possible interventions to limit severe damage in acute neurological disorders.

BACKGROUND: Vitamin E (alpha-tocopherol acetate, AT) diminishes the antiproliferative effect of tamoxifen on breast cancer cells in vitro. METHODS: A prospective study of seven women taking tamoxifen for adjuvant therapy of breast cancer. Four who were already taking AT supplements had random core biopsies of the normal breast and again 30 days after discontinuing AT. Three who were not on AT had biopsies before and after adding AT 400 mg for 30 days. Biopsies were stained for estrogen receptor (ER) and the mitogen-activated protein kinase p-ERK. Tissue extracts were assayed for p-ERK by enzyme-linked immunosorbent assay. Serum levels of alpha-tocopherol and tamoxifen were measured. RESULTS: Five out of seven patients had lower tamoxifen levels while taking AT, four of these went to subtherapeutic levels. Biopsies showed 23% of ductal cells were ER positive when patients were off AT and 70% on AT (P = 0.02). P-ERK staining was 21% off AT and 82% on AT. Five of seven patients had significantly higher tissue p-ERK when on AT. CONCLUSIONS: Biomarkers of estrogen-stimulation (ER, progesterone receptor, and p-ERK) were higher in breast biopsies of women taking vitamin E supplements while taking tamoxifen. Findings suggest that vitamin E supplements may interfere with the therapeutic effects of tamoxifen.

Idebenone, a synthetic analogue of coenzyme Q, attenuates noise-induced hearing loss by virtue of its antioxidant properties. This study involves a guinea pig model of acoustic trauma where the effectiveness of idebenone is analyzed in comparison with Vitamin E (alpha-tocopherol) that exhibits a potent antioxidant activity in the inner ear. Idebenone and vitamin E were injected intraperitoneally 1 h before noise exposure and once daily for three days; functional and morphological studies were then carried out, respectively, by auditory brainstem responses evaluation, scanning electron microscopy and terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling assay identification of missing and apoptotic cells was also performed. The results showed that the protective effects of idebenone and vitamin E were not additive implying that the two antioxidants may share competitive mechanisms.

Different forms of Aluminium (Al) are environmental xenobiotics that induce free radical-mediated cytotoxicity and reproductive toxicity. Vitamin E (alpha -tocopherol) is an antioxidative agent that has been reported to be important for detoxification pathways. This study was thus aimed at elucidating the protective effects of vitamin E towards aluminium toxicity on the histology of the rat testis. Al (5 mg/kg body weight) was administered intraperitoneally in 2 ml saline, either alone or immediately before vitamin E (500 mg/kg body weight), at a different point of abdomen, and the alterations in the testis tissue were analyzed histologically. Seven treated animals were sacrificed for each group, with the testes removed and examined histologically. In the Al-treated group, the germinal epithelium of the seminiferous tubules was thinner in places and spermatids were almost absent; sperm numbers were low and there were no sperm in the lumen. In the Al plus vitamin E rats, there were large numbers of spermatids and sperm in the seminiferous tubule lumen. In the vitamin E alone group, a normal histology was seen. Electron microscopically, in the Al-treated group there were irregularities in the nuclear membrane, some damaged mitochondria, a decrease in the number of ribosomes, and an increase in the number of lysosomes in the sertoli cell cytoplasm. In the primary spermatocyte cytoplasm, there was an increase in the rough endoplasmic reticulum. In the Al plus vitamin E group, the spermatogeneic cells and the sertoli cell cytoplasm showed an almost normal appearance. The ultrastructure of the testis in the vitamin E alone group showed a normal appearance. In conclusion, vitamin E antagonizes the toxic effects of Al at the histological level, thus potentially contributing to an amelioration of the testis histology in the Al-treated rats. The associated biochemical parameters merit further investigation.

Developmental ethanol exposure leads to a variety of abnormalities in the central nervous system (CNS). Mechanisms proposed as underlying these effects include alterations of protective antioxidant support, increased generation of harmful free radicals, and altered expression of apoptosis-related proteins. In prior studies, exogenous antioxidant application has been found to reduce ethanol neurotoxicity, but the mechanisms by which this protection is afforded have not been defined. This study was designed to investigate the interactions between ethanol and the antioxidant vitamin E (alpha-tocopherol), with respect to neuronal survival and levels of proteins related to the Bcl-2 survival-regulatory gene family. Neonatal rat cerebellar granule cell cultures were used as a model system. It was found that ethanol significantly impaired neuronal survival in these preparations, and that survival in the presence of ethanol was enhanced by inclusion of vitamin E in the culture medium. This elevated survival was paralleled by increased levels of anti-apoptotic proteins (e.g., Bcl-2, Bcl-xl, activated Akt kinase), and concurrent downregulation of pro-apoptotic proteins (e.g., Bcl-xs). These results suggest that such alterations may represent an important mechanism whereby antioxidants protect against the neurotoxic effects of ethanol in the developing CNS. The possible manner by which these changes are effected are considered.

BACKGROUND: Radiotherapy, as a method of treatment of cervical and uterine cancers, may induce severe late-onset vaginal side effects. Unfortunately, little evidence on the management of adverse effects has been presented. This study aimed to evaluate the available interventions which reduce symptoms of vaginitis and vaginal atrophy by improving dyspareunia, mucosal inflammation, vaginal pH and vaginal dryness in women who have undergone brachytherapy or radiotherapy due to uterine or cervical malignancies. MATERIALS AND METHODS: A comprehensive literature search was performed following PRISMA guidelines. The systematic search was conducted using electronic databases, namely Scopus, Web of Science and PubMed, between October and November 2020 to identify randomized controlled trials (RCT) and, prospective randomized studies (PRS). RESULTS: The analyzed population consists of 376 patients with uterine or cervical cancer, treated with hyaluronic acid, vitamin A, vitamin E, alpha-tocopherol acetate and dienestrol. Intervention with HA along with vitamin A and vitamin E revealed advantage in endpoints such as reduced dyspareunia, vaginal mucosal inflammation, vaginal dryness, bleeding, fibrosis and cellular atypia. Administration of alpha-tocopherol acetate reduced vaginal mucosal inflammation and improved vaginal acanthosis, whereas dienestrol resulted in reduced dyspareunia, vaginal caliber and bleeding. CONCLUSIONS: Vaginal suppositories were found to be clinically effective at the management of late-onset vulvovaginal side effects after radiotherapy.

Several clinical studies have proposed a protective role for vitamin E (α-tocopherol) against contrast-induced acute kidney injury (CIAKI). The aim of study was to assess the effects of vitamin E for the prevention of CIAKI. A systematic review and meta-analysis was conducted using MEDLINE, EMBASE, and the Cochrane Central Register of Controlled Trials. Randomized controlled trials (RCTs) reporting the effects of vitamin E on CIAKI development and measurements of renal function were included. Four trials including 623 participants were analyzed in the meta-analysis. All participants received intravenous hydration in addition to vitamin E or placebo. The incidence of the vitamin E group (5.8%) was lower than that of the control group (15.4%). Compared with the control, vitamin E significantly reduced the risk ratio (RR) of CIAKI by 62% (0.38; 95% confidence interval [CI], 0.22, 0.63; P < 0.010). In addition, vitamin E reduced serum creatinine (SCr) increase after contrast administration (standardized mean difference [SMD], -0.27; 95% CI, -0.49, -0.06; P = 0.010). However, changes in glomerular filtration rate (GFR) after contrast administration were not significantly different between vitamin E and the control group (SMD, 0.21; 95% CI, -0.01, 0.43; P = 0.060). Heterogeneity within the available trials was not observed. Our meta-analysis provides evidence that vitamin E plus hydration significantly reduced the risk of CIAKI in patients with renal impairment compared with hydration alone. © 2017 The Korean Academy of Medical Sciences.

BACKGROUND: Vitamin E occurs naturally in the diet. It has several biological activities, including functioning as an antioxidant to scavenge toxic free radicals. Evidence that free radicals may contribute to the pathological processes behind cognitive impairment has led to interest in the use of vitamin E supplements to treat mild cognitive impairment (MCI) and Alzheimer's disease (AD). This is an update of a Cochrane Review first published in 2000, and previously updated in 2006 and 2012. OBJECTIVES: To assess the efficacy of vitamin E in the treatment of MCI and dementia due to AD. SEARCH METHODS: We searched the Specialized Register of the Cochrane Dementia and Cognitive Improvement Group (ALOIS), the Cochrane Library, MEDLINE, Embase, PsycINFO, CINAHL, LILACS as well as many trials databases and grey literature sources on 22 April 2016 using the terms: "Vitamin E", vitamin-E, alpha-tocopherol. SELECTION CRITERIA: We included all double-blind, randomised trials in which treatment with any dose of vitamin E was compared with placebo in people with AD or MCI. DATA COLLECTION AND ANALYSIS: We used standard methodological procedures according to the Cochrane Handbook for Systematic Reviews of Interventions. We rated the quality of the evidence using the GRADE approach. Where appropriate we attempted to contact authors to obtain missing information. MAIN RESULTS: Four trials met the inclusion criteria, but we could only extract outcome data in accordance with our protocol from two trials, one in an AD population (n = 304) and one in an MCI population (n = 516). Both trials had an overall low to unclear risk of bias. It was not possible to pool data across studies owing to a lack of comparable outcome measures.In people with AD, we found no evidence of any clinically important effect of vitamin E on cognition, measured with change from baseline in the Alzheimer's Disease Assessment Scale - Cognitive subscale (ADAS-Cog) over six to 48 months (mean difference (MD) -1.81, 95% confidence interval (CI) -3.75 to 0.13, P = 0.07, 1 study, n = 272; moderate quality evidence). There was no evidence of a difference between vitamin E and placebo groups in the risk of experien

BACKGROUND: Vitamin E is a dietary compound that functions as an antioxidant scavenging toxic free radicals. Evidence that free radicals may contribute to the pathological processes of cognitive impairment including Alzheimer's disease has led to interest in the use of vitamin E in the treatment of mild cognitive impairment (MCI) and Alzheimer's dementia (AD). OBJECTIVES: To assess the efficacy of vitamin E in the treatment of AD and prevention of progression of MCI to dementia. SEARCH METHODS: The Specialized Register of the Cochrane Dementia and Cognitive Improvement Group (ALOIS), The Cochrane Library, MEDLINE, EMBASE, PsycINFO, CINAHL, LILACS as well as many trials databases and grey literature sources were searched on 25 June 2012 using the terms: "Vitamin E", vitamin-E, alpha-tocopherol. SELECTION CRITERIA: All unconfounded, double-blind, randomised trials in which treatment with vitamin E at any dose was compared with placebo for patients with AD and MCI. DATA COLLECTION AND ANALYSIS: Two review authors independently applied the selection criteria and assessed study quality and extracted and analysed the data. For each outcome measure data were sought on every patient randomised. Where such data were not available an analysis of patients who completed treatment was conducted. It was not possible to pool data between studies owing to a lack of comparable outcome measure. MAIN RESULTS: Only three studies met the inclusion criteria: two in an AD population and one in an MCI population. In the first of the AD studies (Sano 1996) the authors reported some benefit from vitamin E (2000 IU/day) with fewer participants reaching an end point of death, institutionalisation, change to a Clinical Dementia Rating (CDR) of three, or loss of two basic activities of daily living within two years. Of patients completing treatment, 58% (45/77) on vitamin E compared with 74% (58/78) on placebo reached one of the end points (odds ratio (OR) 0.49; 95% confidence interval (CI) 0.25 to 0.96). The second AD treatment study (Lloret 2009) explored the effects of vitamin E (800 IU/day) on cognitive progression in relation to oxidative stress levels. Patients whose oxidative stress m

BACKGROUND: Vitamin E is a dietary compound that functions as an antioxidant scavenging toxic free radicals. Evidence that free radicals may contribute to the pathological processes of cognitive impairment including Alzheimer's disease (AD) has led to interest in the use of Vitamin E in the treatment of Alzheimer's disease and Mild Cognitivie Impairment (MCI). OBJECTIVES: To assess the efficacy of Vitamin E in the treatment of Alzheimer's disease and prevention of progression of Mild Cognitive Impairment to Alzheimer's disease. SEARCH STRATEGY: The Cochrane Dementia and Cognitive Improvement's Specialized Register was searched on 8 January 2007 using the following terms: "Vitamin E", vitamin-E, alpha-tocopherol. The CDCIG Registers contains records from major health care databases and ongoing trial databases and is updated regularly. SELECTION CRITERIA: All unconfounded, double blind, randomized trials in which treatment with Vitamin E at any dose was compared with placebo for patients with Alzheimer's disease or Mild Cognitive Impairment. DATA COLLECTION AND ANALYSIS: Two reviewers independently applied the selection criteria and assessed study quality and extracted and analysed the data. For each outcome measure data were sought on every patient randomized. Where such data were not available an analysis of patients who completed treatment was conducted. MAIN RESULTS: Only 2 studies met the inclusion criteria. The primary outcome used in the AD study was survival time to the first of 4 endpoints: death, institutionalisation, loss of 2 out of 3 basic activities of daily living and severe dementia (defined as a global Clinical Dementia Rating of 3). The investigators reported the total numbers in each group who reached the primary endpoint within two years for participants completing the study ("completers"). There appeared to be some benefit from Vitamin E with fewer participants reaching endpoint - 58% (45/77) of completers compared with 74% (58/78) - a Peto odds ratio of 0.49, 95% confidence interval 0.25 to 0.96.However, more participants taking Vitamin E suffered a fall (12/77 compared with 4/78; odds ratio 3.07, 95% CI 1.09 to 8.62). It was not possible to