Vitamin E (α-tocopherol) consumption influences gut microbiota composition

Choi Y, Lee S, Kim S, Lee J, Ha J, Oh H, Lee Y, Kim Y, Yoon Y

Int J Food Sci Nutr. 2019 Jul 12:1-5. doi: 10.1080/09637486.2019.1639637. [Epub ahead of print]

Abstract

This study evaluated if vitamin E consumption affects gut microbiota. Mice were grouped into control, low vitamin E (LV), and high vitamin E (HV). LV and HV were fed DL-α-tocopherol at 0.06 mg/20 g and 0.18 mg/20 g of body weight per day, respectively, for 34 days. Body weight of mice was measured before and after vitamin E treatment. Animals were sacrificed, liver, spleen, small intestine and large intestine collected, and weight and length were measured. Composition of gut microbiota was determined by microbiome analysis. Spleen weight index of LV was the highest. However, liver weight indices and intestinal lengths were not different. Body weights of LV group were higher than those of control. Ratio of Firmicutes to Bacteroidetes was different in LV compared to control and HV. These results indicate that low-level consumption of vitamin E increases spleen and body weight, and changes gut microbiota.

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Trolox-induced cardiac differentiation is mediated by the inhibition of Wnt/β-catenin signaling in human embryonic stem cells

Choe MS, Yeo HC, Bae CM, Han HJ, Baek KM, Kim JS, Lim KS, Shin IS, Chang WC, Yun SP, Lee HJ, Lee MY

Cell Biol Int. 2019 Jul 10. doi: 10.1002/cbin.11200. [Epub ahead of print]

Abstract

Cardiac differentiation of human pluripotent stem cells may be induced under chemically defined conditions, wherein the regulation of Wnt/β-catenin pathway is often desirable. Here, we examined the effect of trolox, a vitamin E analog, on the cardiac differentiation of human embryonic stem cells (hESCs). Trolox significantly enhanced cardiac differentiation in a time- and dose-dependent manner after the mesodermal differentiation of hESCs. Trolox promoted hESC cardiac differentiation through its inhibitory activity against the Wnt/β-catenin pathway. This study demonstrates an efficient cardiac differentiation method and reveals a novel Wnt/β-catenin regulator.

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Beneficial effects of δ-tocotrienol against oxidative stress in osteoblastic cells: studies on the mechanisms of action

Casati L, Pagani F, Limonta P, Vanetti C, Stancari G, Sibilia V

Eur J Nutr. 2019 Jul 6. doi: 10.1007/s00394-019-02047-9. [Epub ahead of print]

Abstract

PURPOSE:

Natural antioxidants are considered as promising compounds in the prevention/treatment of osteoporosis. We studied the ability of purified δ-tocotrienol (δ-TT) isolated from a commercial palm oil (Elaeis guineensis) fraction to protect osteoblast MC3T3-E1 and osteocyte MLO-Y4 cells against tert-butyl hydroperoxide (t-BHP)-induced oxidative damage and the mechanisms involved in its protective action in MC3T3-E1.

METHODS:

MC3T3-E1 and MLO-Y4 cells were treated with δ-TT (1.25-20 µg/ml for 2 h) followed by t-BHP at 250 µM or 125 µM for 3 h, respectively. MTT test was used to measure cell viability. Apoptotic cells were stained with Hoechst-33258 dye. Intracellular ROS levels were measured by dichlorofluorescein CM-DCFA. The OPT fluorimetric assay was used to detect the reduced glutathione to oxidized glutathione ratio (GSH/GSSG) contents.

RESULTS:

δ-TT significantly prevented the effects of t-BHP on cell viability and apoptosis reaching a maximum protective activity at 10 and 5 µg/ml in MC3T3-E1 and MLO-Y4 cells, respectively. This protective effect was due to a reduction of intracellular ROS levels and an increase in the defense systems shown by the increase in the GSH/GSSG. GSH loss induced by an inhibitor of GSH synthesis significantly reduced the δ-TT-positive effect on ROS levels. δ-TT prevention of oxidative damage was completely removed by combined treatment with the specific inhibitors of PI3K/AKT (LY294002) and Nrf2 (ML385).

CONCLUSIONS:

The δ-TT protective effect against oxidative damage in MC3T3-E1 cells is due to a reduction of intracellular ROS levels and an increase of the GSH/GSSG ratio, and involves an interaction between the PI3K/Akt-Nrf2 signaling pathways.

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Gamma radiation-induced crosslinked composite membranes based on polyvinyl alcohol/chitosan/AgNO3/vitamin E for biomedical applications

Nasef SM, Khozemy EE, Kamoun EA, El-Gendi H

Int J Biol Macromol. 2019 Jul 5;137:878-885. doi: 10.1016/j.ijbiomac.2019.07.033. [Epub ahead of print]

Abstract

Crosslinked hydrogel composite membranes based on polyvinyl alcohol (PVA) and chitosan-loaded AgNO3 and vitamin E were prepared using gamma irradiation. Chitosan has been used as antimicrobial blend materials to provide further biocompatibility for the prepared composite hydrogel membranes. The crosslinking reaction between PVA and chitosan owing to gamma irradiation was verified and characterized by FTIR analysis, while the morphology of hydrogel composite membranes was investigated by SEM. Important parameters affecting on hydrogel membranes formation, such as copolymer concentration, irradiation dose, AgNO3 concentration, plasticizer, and vitamin E of PVA/chitosan membranes were evaluated and discussed in details. In addition, the mechanical and thermal properties of hydrogel composite membranes were examined to evaluate the possibility of its application for wound dressings. The results revealed that the gelation (%) of hydrogel membranes increased dramatically with PVA composition, irradiation dose and glycerol content up to 20%; however, it decreased with AgNP incorporation due to the viscosity of copolymer composition is hyper-increased. The swelling ratio of composed hydrogel membranes decreased notably with increasing the radiation dose and incorporation of AgNP, due to reducing of the crosslinking degree of formed hydrogel membranes. PVA-Cs-Ag composed hydrogel membranes showed significant antimicrobial activity in particular against Streptococcus mutans due to the presence of AgNP in membranes, compared to other bacteria and fungi microbes. Thus, the PVA/chitosan/AgNO3-Vit.E hydrogel composite membranes showed satisfactory properties for use as wound dressing materials.

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Dietary vitamin E and C intake is inversely associated with the severity of nonalcoholic fatty liver disease

Ivancovsky-Wajcman D, Fliss-Isakov N, Salomone F, Webb M, Shibolet O, Kariv R, Zelber-Sagi S

Dig Liver Dis. 2019 Jul 4. pii: S1590-8658(19)30662-0. doi: 10.1016/j.dld.2019.06.005. [Epub ahead of print]

Abstract

BACKGROUND & AIMS:

Although antioxidants have a protective potential in nonalcoholic fatty liver disease (NAFLD) and steatohepatitis (NASH), there is limited evidence regarding the role of dietary intake of antioxidants. The aim was to test the association between dietary vitamins E and C intake and NAFLD, NASH and fibrosis markers.

METHODS:

Cross-sectional study of a large cohort of subjects undergoing colonoscopy. The presence of NAFLD was evaluated by ultrasonography. The level of steatosis was defined using SteatoTest, moderate-severe NASH using new quantitative NashTest and borderline-significant fibrosis ≥ F1-F2 using FibroTest. Nutritional intake was measured by food frequency questionnaire (FFQ).

RESULTS:

Overall, 789 subjects were included (52.6% men, age 58.83 ± 6.58 years), 714 had reliable FibroMax. Adjusting for BMI, dietary and lifestyle factors, the upper tertile of vitamin E intake/1000 Kcal was associated with lower odds of NASH (OR = 0.64, 0.43-0.94, P = 0.024). There was an inverse association between reaching the recommended vitamin E intake and NASH (OR = 0.48, 0.30-0.77, P = 0.002). The upper tertile of vitamin C intake/1000 Kcal was associated with lower odds of NAFLD and NASH (OR = 0.68, 0.47-0.99, P = 0.045; OR = 0.57, 0.38-0.84, P = 0.004, respectively). Both vitamins were related with the level of steatosis according to SteatoTest.

CONCLUSION:

Vitamin E and C intake may be protective from NAFLD-related liver damage.

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Evaluation of the biocompatibility and skin hydration potential of vitamin E-loaded lipid nanosystems formulations: In vitro and human in vivo studies

Vaz S, Silva R, Amaral MH, Martins E, Sousa Lobo JM, Silva AC

Colloids Surf B Biointerfaces. 2019 Jul 1;179:242-249. doi: 10.1016/j.colsurfb.2019.03.036. Epub 2019 Apr 3.

Abstract

Lipid-based nanosystems, such as nanostructured lipid carriers (NLC) and nanoemulsions (NE) have been described as promising alternatives to conventional formulations for increase skin hydration. Besides, these systems have been used as efficient vehicles for lipophilic molecules that improve skin properties (e.g. vitamin E). In this study, we performed comparative investigations between hydrogels formulations containing vitamin E-loaded NLC (HG-NLCVE) and vitamin E-loaded nanoemulsion (HG-NEVE). The experiments started with particle size measurements, which showed no significant differences between nanoparticles/nanodroplets sizes after incorporation in the hydrogel net (386 nm vs. 397 nm for HG-NLCVE and 402 nm vs. 514 nm for HG-NEVE). Afterwards, in vitro biocompatibility studies in human keratinocytes were carried out, being observed that the lipid-based nanosystems were more cytotoxic for the cells before incorporation in the hydrogel. Finally, the formulations hydration potential and sensory attributes for skin application were evaluated by in vitro occlusion tests and in vivo human experiments. The results showed that the HG-NLCVE exhibited the best occlusive properties, whereas the HG-NEVEperformed a faster skin hydration effect. Furthermore, the latter was selected as the most attractive for skin application, although the HG-NLCVE was described as more suitable to obtain a long-lasting effect. This study demonstrated the in vitro and in vivo safety and hydration potential of hydrogels containing vitamin E-loaded lipid-based nanosystems. These results establish a basis to assess the cutaneous use of these systems, despite more in vivo experiments, for longer periods and in more volunteers, are required before commercialization.

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Vitamin E modifies high-fat diet-induced reduction of seizure threshold in rats: Role of oxidative stress

Alzoubi KH, Hasan ZA, Khabour OF, Mayyas FA, Al Yacoub ON, Banihani SA, Alomari MA, Alrabadi NN

Physiol Behav. 2019 Jul 1;206:200-205. doi: 10.1016/j.physbeh.2019.04.011. Epub 2019 Apr 13.

Abstract

There is increasing evidence that oxidative stress is a causal factor in different neurodegenerative disorders such as Alzheimer’s disease and epilepsy. High-fat diet (HFD) has been shown to induce oxidative stress and neuronal damage that may increase susceptibility to seizures. The present study was undertaken to investigate the relationships between vitamin E, a potent antioxidant, HFD, and chemically induced seizures, using the PTZ seizure model in rats. Animals were randomly assigned into four groups: control, HFD, vitamin E (Vit E), and high-fat diet with vitamin E (HFD + Vit E) group. Vitamin E and/or HFD were administered to animals for 6 weeks. Thereafter, PTZ seizure threshold was measured in control and treated rats, and different brain regions were analyzed for levels of oxidative stress biomarkers. Current results revealed a significant reduction in PTZ seizure threshold in rats consuming HFD, which could be prevented by vitamin E supplement. Alongside, vitamin E supplement prevented HFD induced changes in oxidative stress biomarkers and capacity enzymes. Therefore, current results suggest that prolonged consumption of HFD increases susceptibility to PTZ induced seizures, which may be related to HFD induced oxidative stress. This increase in the PTZ susceptibility could be prevented by the administration of vitamin E, probably through its antioxidant effect, particularly at the brain hippocampal region.

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Glutathione peroxidase 4 and vitamin E control reticulocyte maturation, stress erythropoiesis and iron homeostasis

Altamura S, Vegi NM, Hoppe PS, Schroeder T, Aichler M, Walch A, Okreglicka K, Hültner L, Schneider M, Ladinig C, Kuklik-Roos C, Mysliwietz J, Janik D, Neff F, Rathkolb B, Hrabé de Angelis M, Buske C, da Silva AR, Muedder K, Conrad M, Ganz T, Kopf M, Muckenthaler MU, Bornkamm GW

Haematologica. 2019 Jun 27. pii: haematol.2018.212977. doi: 10.3324/haematol.2018.212977. [Epub ahead of print]

Abstract

Glutathione peroxidase 4 (GPX4) is unique as it is the only enzyme that can prevent detrimental lipid peroxidation in vivo by reducing lipid peroxides to the respective alcohols thereby stabilizing oxidation products of unsaturated fatty acids. During reticulocyte maturation, 15-lipoxygenase-mediated lipid peroxidation in humans and rabbits and by 12/15-lipoxygenase (ALOX15) in mice had been considered as the initiating event for the elimination of mitochondria which is now known to occur through mitophagy. Yet, genetic ablation of the Alox15 gene in mice failed to provide evidence for this hypothesis. We designed a different genetic approach to tackle this open conundrum. Since either other lipoxygenases or non-enzymatic autooxidative mechanisms may compensate for the loss of Alox15, we asked whether ablation of GPX4 in the hematopoietic system would result in perturbation of reticulocyte maturation. Quantitative assessment of erythropoiesis indices in the blood, bone marrow and spleen of chimeric mice with GPX4 ablated in hematopoietic cells revealed anemia with an increase in the fraction of erythroid precursor cells and reticulocytes. Additional dietary vitamin E depletion strongly aggravated the anemic phenotype. Despite strong extramedullary erythropoiesis reticulocytes failed to mature and accumulated large autophagosomes with engulfed mitochondria. GPX4-deficiency in hematopoietic cells led to systemic hepatic iron overload and simultaneous severe iron demand in the erythroid system. Despite extremely high erythropoietin and erythroferrone levels in the plasma, hepcidin expression remained unchanged. Conclusively, perturbed reticulocyte maturation in response to GPX4 loss in hematopoietic cells thus causes ineffective erythropoiesis, a phenotype partially masked by dietary vitamin E supplementation.

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Antagonistic effect of vitamin E on nAl2O3-induced exacerbation of Th2 and Th17-mediated allergic asthma via oxidative stress

Cui H, Huang J, Lu M, Zhang Q, Qin W, Zhao Y, Lu X, Zhang J, Xi Z, Li R

Environ Pollut. 2019 Jun 26;252(Pt B):1519-1531. doi: 10.1016/j.envpol.2019.06.092. [Epub ahead of print]

Abstract

Some basic research has shown that nanomaterials can aggravate allergic asthma. However, its potential mechanism is insufficient. Based on the research that alumina nanopowder (nAl2O3) has been reported to cause lung tissue damage, the purpose of this study was to explore the relationship between nAl2O3 and allergic asthma as well as its molecular mechanism. In this study, Balb/c mice were sensitized with ovalbumin (OVA) to construct the allergic asthma model while intratracheally administered 0.5, 5 or 50 mg kg-1·day-1 nAl2O3 for 3 weeks. It was observed that exposure to nAl2O3 exacerbated airway hyperresponsiveness (AHR), airway remodeling, and inflammation cell infiltration, leading to lung function damage in mice. Results revealed that nAl2O3 could increase ROS levels and decrease GSH levels in lung tissue, promote the increases of the T-IgE, TGF-β, IL-1β and IL-6 levels, stimulate the overexpression of transcription factors GATA-3 and RORγt, decrease the levels of IFN-γ and IL-10 and increase the levels of IL-4 and IL-17A, resulting in the imbalance of Th1/Th2 and Treg/Th17 immune responses. In addition, antioxidant Vitamin E (Vit E) could alleviate asthma-like symptoms through blocking oxidative stress. The study displayed that exposure of nAl2O3 deteriorated allergic asthma through promoting the imbalances of Th1/Th2 and Treg/Th17.

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Association of serum γ-tocopherol levels with mortality: the Multiethnic Cohort Study

Chai W, Maskarinec G, Franke AA, Monroe KR, Park SY, Kolonel LN, Wilkens LR, Le Marchand L, Cooney RV

Eur J Clin Nutr. 2019 Jun 26. doi: 10.1038/s41430-019-0460-7. [Epub ahead of print]

Abstract

BACKGROUND/OBJECTIVES:

γ-Tocopherol has unique properties that protect against nitrogen oxide-mediated cellular damage. To elucidate the potential role of γ-tocopherol in the aging process, we examined the associations of serum γ-tocopherol levels with all-cause and cause-specific mortality.

SUBJECTS/METHODS:

Among participants in the biorepository subcohort of the Multiethnic Cohort Study, pre-cancer diagnostic serum γ-tocopherol levels were measured in a subset of 3904 men and 4461 women. Of these, 22.7% of men and 13.5% of women died during a mean follow-up time of 9.6 ± 2.6 years. Hazard ratios (HRs) and 95% confidence intervals (95% CIs) for mortality associated with γ-tocopherol were estimated by Cox proportional hazards regression.

RESULTS:

Positive associations of serum γ-tocopherol with all-cause, cancer, and cardiovascular disease mortality (CVD) (Ptrend < 0.05) were detected after adjusting for age, race/ethnicity, and serum cholesterol levels. The respective HRs (95% CIs) for the highest versus the lowest sex-specific γ-tocopherol quartile were 1.43 (1.17-1.74), 1.79 (1.22-2.64), and 1.52 (1.10-2.11) for men and 1.58 (1.25-2.00), 1.59 (1.05-2.41), and 1.59 (1.07-2.37) for women. Associations remained significant for all-cause mortality among women after further adjusting for smoking variables and history of cancer, CVD, diabetes, and hypertension at cohort entry (highest vs. lowest γ-tocopherol quartile: HR = 1.38; 95% CI = 1.08-1.75; Ptrend = 0.005). Overall, associations with all-cause mortality were consistent across race/ethnicity and were significant in three of ten sex-specific racial/ethnic groups in the fully adjusted models, with no interactions between ethnicity and γ-tocopherol.

CONCLUSIONS:

The positive association between γ-tocopherol and mortality suggests a potential physiological role for γ-tocopherol in response to pathological conditions.

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