Vitamin E supplementation in chronically hemodialyzed patients – influence on blood hemoglobin and plasma (anti)oxidant status

Ruskovska T, Pop-Kostova A, Hjm Jansen E, Antarorov R, Gjorgoski I

Int J Vitam Nutr Res. 2019 Feb 27:1-10. doi: 10.1024/0300-9831/a000471. [Epub ahead of print]

Abstract

BACKGROUND:

Disturbed oxidant/antioxidant status is involved in pathogenesis of anemia in end stage renal disease. There is evidence that vitamin E supplementation can increase blood hemoglobin in chronically hemodialyzed patients. However, the interindividual variation in response to the supplementation has not been fully addressed.

METHODS:

24 chronically hemodialyzed patients were supplemented with vitamin E (400 IU/day) in a period of two months. They had already been treated with erythropoiesis stimulating agents (ESA) and iron on a long-term basis, which was continued during the study period. A group of 20 healthy volunteers served as control subjects. Complete blood count, general biochemistry assays, the redox status by total thiols, oxidative stress by reactive oxygen metabolites, antioxidant status by biological antioxidant potential, and vitamin E (α- and γ- tocopherol) were measured before the start of supplementation, one month and two months later.

RESULTS:

Overall, the vitamin E supplementation did not cause an increase of blood hemoglobin, hematocrit or red blood cells. However, 50 % of the patients with basal blood hemoglobin below 12.0 g/dL (N = 10) responded to the supplementation with its continuous increase. In addition, vitamin E exhibited a slight prooxidant effect only in the subgroup of patients with basal blood hemoglobin of ≥ 12.0 g/dL, two months after the start of supplementation (decreased total thiols: 300 ± 31 vs. 277 ± 36 µmol/L, p < 0.05; increased reactive oxygen metabolites: 183 ± 140 vs. 287 ± 112 CARR U, p > 0.05; decreased biological antioxidant potential: 2278 ± 150 vs. 2171 ± 126 µEq/L, p < 0.025), which coincided with their significantly increased serum α-tocopherol concentrations in comparison to the patients with basal blood hemoglobin below 12.0 g/dL (41.3 ± 7.2 vs. 59.9 ± 19.2 µmol/L, p < 0.025).

CONCLUSIONS:

When treated with ESA and iron on a long-term basis, the response to the vitamin E supplementation in chronically hemodialyzed patients is largely dependent on their basal blood hemoglobin and serum vitamin E concentrations.

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Nutritional modulation of the antioxidant capacities in poultry: the case of vitamin E

Surai PF, Kochish II, Romanov MN, Griffin DK

Poult Sci. 2019 Feb 26. pii: pez072. doi: 10.3382/ps/pez072. [Epub ahead of print]

Abstract

Commercial poultry production is associated with a range of stresses, including environmental, technological, nutritional, and internal/biological ones, responsible for decreased productive and reproductive performance of poultry. At the molecular level, most of them are associated with oxidative stress and damages to important biological molecules. Poultry feed contains a range of feed-derived and supplemented antioxidants and, among them, vitamin E is considered as the “headquarters” of the antioxidant defense network. It is well-established that dietary supplementation of selenium, vitamin E, and carotenoids can modulate antioxidant defenses in poultry. The aim of the present paper is to present evidence related to modulation of the antioxidant capacities in poultry by vitamin E. Using 3 model systems including poultry breeders/males, semen, and chicken embryo/postnatal chickens, the possibility of modulation of the antioxidant defense mechanisms has been clearly demonstrated. It was shown that increased vitamin E supplementation in the breeder’s or cockerel’s diet increased their resistance to various stresses, including high polyunsaturated fatty acids (PUFA), mycotoxin, or heat stress. Increased vitamin E supplementation of poultry males was shown to be associated with significant increases in α-tocopherol level in semen associated with an increased resistance to oxidative stress imposed by various external stressors. Similarly, increased vitamin E concentration in the egg yolk due to dietary supplementation was shown to be associated with increased α-tocopherol concentration in the tissues of the developing embryos and newly hatched chicks resulting in increased antioxidant defenses and decreased lipid peroxidation. Furthermore, increased vitamin E transfer from the feed to egg yolk and further to the developing embryo was shown to be associated with upregulation of antioxidant enzymes reflecting antioxidant system regulation and adaptation. The role of vitamin E in cell signaling and gene expression as well as in interaction with microbiota and maintaining gut health in poultry awaits further investigation.

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Vitamin E consumption and the risk of bladder cancer

Lin JH, Chen SJ, Liu H, Yan Y, Zheng JH

Int J Vitam Nutr Res. 2019 Feb 26:1-8. doi: 10.1024/0300-9831/a000553. [Epub ahead of print]

Abstract

BACKGROUND:

Vitamin E has anti-cancer properties, which was demonstrated mainly due to its antioxidant effect. Several epidemiological studies have investigated the association between vitamin E consumption and the risk of bladder cancer. However, the results were inconsistent. The meta-analysis study aimed to evaluate the association of vitamin E consumption and the risk of bladder cancer.

METHODS:

We conducted a systematic literature search in the electronic databases, which included MEDLINE, EMBASE and the Cochrane Library till 1 January 2016. The pooled relative risk ratios (RRs) with 95% confidence intervals (CIs) were calculated depending on the heterogeneity among studies. Subgroup analysis and sensitivity analysis were also performed. Publication bias was assessed using Begg’s test and Egger’s test.

RESULTS:

A total of 11 prospective studies (3 randomized clinical trials and 8 cohort studies) including 575601 participants were identified to be eligible for our present meta-analysis. The pooled RRs with 95% CI for highest versus lowest vitamin E consumption was 0.89 (0.78-1.00). An inverse linear association between vitamin E consumption and bladder cancer risk was detected in the dose response analysis. The results were also stable in the subgroup analysis and sensitivity analysis. Meanwhile, no obvious publication bias was observed.

CONCLUSIONS:

Our study indicates that vitamin E consumption was inversely associated with the risk of bladder cancer.

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The neuroprotective effect of vitamin E on waterpipe tobacco smoking-induced memory impairment: The antioxidative role

Alzoubi KH, Halboup AM, Alomari MM, Khabour OF

Life Sci. 2019 Feb 25. pii: S0024-3205(19)30140-7. doi: 10.1016/j.lfs.2019.02.050. [Epub ahead of print]

Abstract

AIMS:

Tobacco smoking is associated with a vast range of adverse health effects, including diminished cognitive and anti-oxidative capabilities. Conversely, vitamin E (VitE) is known to enhance data acquisition and retention and hippocampal oxidative defense. No studies, however, examined the protective effect of VitE with tobacco administration. Therefore, this study examined the protective effect of VitE on the cognitive and oxidative debilitating effects induced by waterpipe smoking.

MATERIALS AND METHODS:

Wistar male rats were divided into four groups: waterpipe smoking, VitE, waterpipe combined with VitE, and control group. The exposure to waterpipe and VitE was for one month and then spatial learning and memory were assesses using Radial Arms Water Maze. Additionally, oxidative stress biomarkers (Catalase, GPx, and TBARS, GSH, GSSG, and GSH/GSSG ratio) were assessed in the hippocampus.

KEY FINDINGS:

The results revealed that waterpipe smoking impaired short-term and long-term memory (P < 0.05). Waterpipe smoking reduced activity of catalase (P < 0.05), GPx (P < 0.05) and GSH/GSSG ratio (P < 0.05) in the hippocampus. Administration of VitE prevented memory impairment and alterations in oxidative stress biomarkers.

SIGNIFICANCE:

waterpipe smoking induces short-term and long-term memory impairments, which were prevented by administration of VitE via its anti-oxidative properties.

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The Effect of Lipid Antioxidant α-Tocopherol on Cell Viability and Electrofusion Yield of B16-F1 Cells In Vitro

Kanduser M, Kokalj Imsirovic M, Usaj M

J Membr Biol. 2019 Feb;252(1):105-114. doi: 10.1007/s00232-019-00059-4. Epub 2019 Jan 22.

Abstract

Induced cell fusion is a powerful method for production of hybridoma in biotechnology and cell vaccines in medical applications. Among different alternatives, physical methods have an advantage, as they do not require any additives. Among them electrofusion, an electroporation-based cell fusion method holds a great promise. Electric pulses cause cell membrane permeabilization and due to pore formation bring cell membrane into the fusogenic state. At the same time, however, they compromise cell viability. We used a train of 8 × 100 µs electric pulses, delivered at 1 Hz with strengths ranging from 400 to 1600 V/cm. We evaluated electrofusion efficiency by dual color microscopy. We determined cell viability, because during electroporation reactive oxygen species are generated affecting cell survival. The novelty of our study is evaluation of the effect of lipid antioxidant α-tocopherol on cell fusion yield and cell viability on mouse B16-F1 cells. Pretreatment with α-tocopherol slowed down dynamic of cell fusion shortly after electroporation. Twenty-four hours later, fusion yields between α-tocopherol treated and untreated cells were comparable. The viability of α-tocopherol pretreated cells was drastically improved. Pretreatment of cells with α-tocopherol improved whole electrofusion process by more than 60%. We believe that α-tocopherol holds great promise to become an important agent to improve cell electrofusion method.

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DHA and vitamin E antagonized the Aβ25-35-mediated neuron oxidative damage through activation of Nrf2 signaling pathways and regulation of CD36, SRB1 and FABP5 expression in PC12 cells

Huang X , Zhen J , Dong S , Zhang H , Van Halm-Lutterodt N , Yuan L

Food Funct. 2019 Feb 20;10(2):1049-1061. doi: 10.1039/c8fo01713a.

Abstract

The present study was designed to explore the neuroprotective effects of docosahexaenoic acid (DHA) and/or vitamin E (VE) in vitro. The PC12 cells were pretreated with DHA and/or VE for 4 h, followed by 50 μmol L-1 Aβ25-35 treatments for another 48 h. The cells were then collected and used for the measurements of oxidative stress parameters. Real time-PCR and western blot were applied to measure fatty acid transporters, Nrf2 and its downstream antioxidant targets’ gene and protein expression. Our results indicated that the Aβ25-35 treatment inhibited cellular growth, increased intracellular ROS generation and decreased the mitochondrial membrane potential. The Aβ25-35 treatment decreased the total antioxidant capacity (T-AOC), whereas it increased the MDA levels in neuron cells. Pretreatment of cells with VE or DHA could antagonize the Aβ25-35-mediated cell growth inhibition and mitochondrial membrane potential decline. Activation of the Nrf2 signaling pathway and regulation of CD36, SRB1 and FABP5 expression were observed in DHA- and DHA + VE-pretreated cells. Our results indicated a synergistic effect of DHA and VE in antagonizing the oxidative damage caused by Aβ25-35 in the PC12 cells. The results of the present study will shed light on the application of nutritional intervention for DHA and VE in preventing neuronal damage-related diseases.

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Vitamin E: Regulatory role in the cardiovascular system

Sozen E, Demirel T, Ozer NK

IUBMB Life. 2019 Feb 18. doi: 10.1002/iub.2020. [Epub ahead of print]

Abstract

Cardiovascular disease (CVD) is one of the major causes of morbidity and mortality, all around the world. Vitamin E is an important nutrient influencing key cellular and molecular mechanisms as well as gene expression regulation centrally involved in the prevention of CVD. Cell culture and animal studies have focused on the identification of vitamin E regulated signaling pathways and involvement on inflammation, lipid homeostasis, and atherosclerotic plaque stability. While some of these vitamin E functions were verified in clinical trials, some of the positive effects were not translated into beneficial outcomes in epidemiological studies. In recent years, the physiological metabolites of vitamin E, including the liver derived (long- and short-chain) metabolites and phosphorylated (α-, γ-tocopheryl phosphate) forms, have also provided novel mechanistic insight into CVD regulation that expands beyond the vitamin E precursor. It is certain that this emerging insight into the molecular and cellular action of vitamin E will help to design further studies, either in animal models or clinical trials, on the reduction of risk for CVDs. This review focuses on vitamin E-mediated preventive cardiovascular effects and discusses novel insights into the biology and mechanism of action of vitamin E metabolites in CVD.

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The Effectiveness of Vitamin E Treatment in Alzheimer’s Disease

Lloret A, Esteve D, Monllor P, Cervera-Ferri A, Lloret A

Int J Mol Sci. 2019 Feb 18;20(4). pii: E879. doi: 10.3390/ijms20040879.

Abstract

Vitamin E was proposed as treatment for Alzheimer’s disease many years ago. However, the effectiveness of the drug is not clear. Vitamin Eis an antioxidant and neuroprotector and it has anti-inflammatory and hypocholesterolemic properties, driving to its importance for brain health. Moreover, the levels of vitamin E in Alzheimer’s disease patients are lower than in non-demented controls. Thus, vitamin E could be a good candidate to have beneficial effects against Alzheimer’s. However, evidence is consistent with a limited effectiveness of vitamin E in slowing progression of dementia; the information is mixed and inconclusive. The question is why does vitamin E fail to treat Alzheimer’s disease? In this paper we review the studies with and without positive results in Alzheimer’s disease and we discuss the reasons why vitamin E as treatment sometimes has positive results on cognition but at others, it does not.

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Serum vitamin E as a significant prognostic factor in patients with dyslipidemia disorders

Barzegar-Amini M, Ghazizadeh H, Seyedi SMR, Sadeghnia HR, Mohammadi A, Hassanzade-Daloee M, Barati E, Kharazmi-Khorassani S, Kharazmi-Khorassani J, Mohammadi-Bajgiran M, Tavallaie S, Ferns GA, Mouhebati M, Ebrahimi M, Tayefi M, Ghayour-Mobarhan M

Diabetes Metab Syndr. 2019 Jan - Feb;13(1):666-671. doi: 10.1016/j.dsx.2018.11.034. Epub 2018 Nov 13.

Abstract

OBJECTIVES:

Obesity and overweight are among the main causes of cardiovascular disease (CVD) mortality. Dyslipidemia, fatty liver index, is strongly related to CVD. Vitamin E as an antioxidant protects the hepatic cells against oxidative stress and prevents fatty liver disease. The aim of the current study is to evaluate the relationship between anthropometric parameters and fasted lipid profile with serum vitamin Elevels.

STUDY DESIGN:

A randomized trial was designed based on data from the Mashhad stroke and heart atherosclerotic disorders (MASHAD: 2010-2020).

METHODS:

363 CVD subjects (173 males and 190 females) was selected at random, among 9704 subjects in three regions of Mashhad, northeast of Iran to investigate the specific correlations among their serum vitamin E, lipid profile (TG, HDL-C, LDL-C and TC), and anthropometric features (height, weight, BMI, hip and waist circumferences.

RESULT:

The results indicated the significant relationships between vitamin E, and fasting serum lipid profile in subjects. Serum vitamin Ewas negatively correlated to TC, TG, and LDL-C and positively related to HDL-C. Also, statistically negative correlations were found between vitamin E and anthropometric parameters (weight, waist and hip circumference, middle Arm, and Systolic Blood Pressure). Moreover, vitamin E ratios such as vitamin E/(TC + TG) and vitamin E/TC values as standardized vitamin E, had significant negative correlation with BMI, the whole of anthropometric parameters, and dyslipidemia risk factors including TC, TG and LDL-C.

CONCLUSION:

We found that vitamin E profile was significantly lower in the dyslipidemia subjects. It is generally suggested that vitamin E monitoring might be used as a useful prognostic and therapeutic agent in dyslipidemia disorder.

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