Effect of vitamin E on stroke-associated pneumonia

Hongwei Shen, Bingyan Zhan

J Int Med Res . 2020 Sep;48(9):300060520949657. doi: 10.1177/0300060520949657.

Abstract

Objective: To study the role of vitamin E in stroke-associated pneumonia.

Methods: We selected 183 patients with stroke-related pneumonia who were divided into different nutrition groups according to the Mini Nutritional Assessment score. Patients were then administered different doses of vitamin E.

Results: CD55 and CD47 levels in patients taking vitamin E across different nutrition score groups were better than those in patients who did not use vitamin E. The levels of CD55 and CD47 and the duration of hospitalization were better in the high-dose vitamin E group than in the low-dose vitamin E group.

Conclusion: Vitamin E may have an auxiliary therapeutic effect in patients with stroke-associated pneumonia.

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A Mechanical Mechanism for Vitamin E Acetate in E-cigarette/Vaping-Associated Lung Injury

Mitchell DiPasquale, Omotayo Gbadamosi, Michael H L Nguyen, Stuart R Castillo, Brett W Rickeard, Elizabeth G Kelley, Michihiro Nagao, Drew Marquardt

Chem Res Toxicol . 2020 Sep 21;33(9):2432-2440. doi: 10.1021/acs.chemrestox.0c00212. Epub 2020 Sep 4.

Abstract

The outbreak of electronic-cigarette/vaping-associated lung injury (EVALI) has made thousands ill. This lung injury has been attributed to a physical interaction between toxicants from the vaping solution and the pulmonary surfactant. In particular, studies have implicated vitamin E acetate as a potential instigator of EVALI. Pulmonary surfactant is vital to proper respiration through the mechanical processes of adsorption and interface stability to achieve and maintain low surface tension at the air-liquid interface. Using neutron spin echo spectroscopy, we investigate the impact of vitamin E acetate on the mechanical properties of two lipid-only pulmonary surfactant mimics: pure 1,2-dipalmitoyl-sn-glycero-3-phosphocholine and a more comprehensive lipid mixture. It was found that increasing vitamin E acetate concentration nonlinearly increased membrane fluidity and area compressibility to a plateau. Softer membranes would promote adsorption to the air-liquid interface during inspiration as well as collapse from the interface during expiration. These findings indicate the potential for the failure of the pulmonary surfactant upon expiration, attributed to monolayer collapse. This collapse could contribute to the observed EVALI signs and symptoms, including shortness of breath and pneumonitis.

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Vitamin E supplementation in people with cystic fibrosis

Peter O Okebukola, Sonal Kansra, Joanne Barrett

Cochrane Database Syst Rev . 2020 Sep 6;9:CD009422. doi: 10.1002/14651858.CD009422.pub4.

Abstract

Background: People with cystic fibrosis are at an increased risk of fat-soluble vitamin deficiency, including vitamin E. Vitamin E deficiency can cause a host of conditions such as haemolytic anaemia, cerebellar ataxia and cognitive difficulties. Vitamin E supplementation is widely recommended for people with cystic fibrosis and aims to ameliorate this deficiency. This is an updated version of the review.

Objectives: To determine the effects of any level of vitamin E supplementation on the frequency of vitamin E deficiency disorders in people with cystic fibrosis.

Search methods: We searched the Cochrane Group’s Cystic Fibrosis Trials Register and also searched international online trial registries for any ongoing clinical trials that were not identified during our register search. Date of last search of the Register: 11 August 2020. Date of last search of international online trial registries: 20 July 2020.

Selection criteria: Randomised controlled trials and quasi-randomised controlled trials comparing any preparation of vitamin E supplementation to placebo or no supplement, regardless of dosage or duration.

Data collection and analysis: Two authors extracted outcome data from each study (published information) and assessed the risk of bias of each included study. They assessed the quality of the evidence using GRADE.

Main results: Four studies with a total of 141 participants were included in the review, two of these were in children (aged six months to 14.5 years), and two did not specify participants’ age. All studies used different formulations and doses of vitamin E for various durations of treatment (10 days to six months). Two studies compared the supplementation of fat-soluble as well as water-soluble formulations to no supplementation in different arms of the same study. A third study compared a water-soluble formulation to a placebo; and in the fourth study a fat-soluble formulation of vitamin E was assessed against placebo. There was limited detail about randomisation and blinding in the included studies which compromises the quality of the evidence base for the review. The heterogeneous mix of the formulations with differing biovailabilities among these studies also limits the generalisability of the data to the wider cystic fibrosis population. None of the studies in either comparison report the review’s primary outcomes of vitamin E total lipid ratio or the incidence of vitamin E-specific deficiency disorders, or the secondary outcomes lung function or quality of life. Water-soluble vitamin E Water-soluble vitamin E may improve serum vitamin E levels compared with control at six months, one study (45 participants), mean difference (MD) 19.74 umol/L (95% confidence interval (CI) 13.48 to 26.00) (low-quality evidence). Similar results were also seen at one month, two studies (32 participants), MD 17.66 umol/L (95% CI 10.59 to 24.74) and at three months, one study (45 participants), MD 11.61 umol/L (95% CI 4.77 to 18.45). Only one study (45 participants) reported weight (secondary outcome of growth and nutritional status) at one and six months, but showed no difference between treatment and control at either time point. Fat-soluble vitamin E Two studies (36 participants) reported higher levels of serum vitamin E at one month with fat-soluble vitamin E compared with control, MD 13.59 umol/L (95% CI 9.52 to 17.66); however, at three months one study (36 participants) showed no difference between treatment and control. No studies in this comparison reported on growth or nutritional status.

Authors’ conclusions: Vitamin E supplementation may lead to an improvement in vitamin E levels in people with cystic fibrosis, although evidence we assessed was low quality. No data on other outcomes of interest were available to allow conclusions about any other benefits of this therapy. In future, larger studies are needed, especially in people already being treated with enteric-coated pancreatic enzymes and supplemented with vitamin E, to look at more specific outcome measures such as vitamin E status, lung function and nutritional status. Future studies could also look at the optimal dose of vitamin E required to achieve maximal clinical effectiveness.

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Does ‘Dry Hit’ vaping of vitamin E acetate contribute to EVALI? Simulating toxic ketene formation during e-cigarette use

Milad Narimani, Gabriel da Silva

PLoS One . 2020 Sep 3;15(9):e0238140. doi: 10.1371/journal.pone.0238140. eCollection 2020.

Abstract

Vitamin E acetate (VEA) is strongly linked to the outbreak of electronic-cigarette or vaping product use-associated lung injury (EVALI). It has been proposed that VEA decomposition to ketene-a respiratory poison that damages lungs at low ppm levels-may play a role in EVALI. However, there is no information available on the temperature at which VEA decomposes and how this correlates with the vaping process. We have studied the temperature-dependent kinetics of VEA decomposition using quantum chemical and statistical mechanical modelling techniques, developing a chemical kinetic model of the vaping process. This model predicts that, under typical vaping conditions, the use of VEA contaminated e-cigarette products is unlikely to produce ketene at harmful levels. However, at the high temperatures encountered at low e-cigarette product levels, which produce ‘dry hits’, ketene concentrations are predicted to reach acutely toxic levels in the lungs (as high as 30 ppm). We therefore hypothesize that dry hit vaping of e-cigarette products containing VEA contributes to EVALI.

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Dose-Dependent Pulmonary Toxicity of Aerosolized Vitamin E Acetate

Shotaro Matsumoto, Xiaohui Fang , Maret G Traber, Kirk D Jones, Charles Langelier, Paula Hayakawa Serpa, Carolyn S Calfee, Michael A Matthay, Jeffrey E Gotts

Am J Respir Cell Mol Biol . 2020 Aug 21. doi: 10.1165/rcmb.2020-0209OC. Online ahead of print.

Abstract

E-cigarette, or vaping, product use-associated lung injury (EVALI) is a syndrome of acute respiratory failure characterized by monocytic and neutrophilic alveolar inflammation. Epidemiological and clinical evidence suggests a role of Vitamin E acetate (VEA) in the development of EVALI, yet it remains unclear whether VEA has direct pulmonary toxicity. To test the hypotheses that aerosolized VEA causes lung injury in mice and directly injures human alveolar epithelial cells, we exposed adult mice and primary human alveolar epithelial type II (AT II) cells to an aerosol of VEA generated by a device designed for vaping oils. Outcome measures in mice included lung edema, bronchoalveolar lavage (BAL) analysis, histology, and inflammatory cytokines; in vitro outcomes included cell death, cytokine release, cellular uptake of VEA, and gene expression analysis. Comparison exposures in both models included the popular nicotine-containing JUUL aerosol. We discovered that VEA caused dose-dependent increases in lung water and BAL protein compared to control and JUUL-exposed mice in association with increased BAL neutrophils, oil-laden macrophages, multinucleated giant cells, and inflammatory cytokines. VEA aerosol was also toxic to AT II cells, causing increased cell death and the release of monocyte and neutrophil chemokines. VEA was directly absorbed by AT II cells, resulting in the differential gene expression of several inflammatory biological pathways. Given the epidemiological and clinical characteristics of the EVALI outbreak, these results suggest that VEA plays an important causal role.

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Serum level and clinical significance of vitamin E in children with allergic rhinitis

Shi-Yi Wang, Yin-Feng Wang, Chun-Chen Pan, Jing-Wu Sun

BMC Pediatr . 2020 Jul 31;20(1):362. doi: 10.1186/s12887-020-02248-w.

Abstract

Background: Allergic rhinitis (AR) is one of the most prevalent allergic diseases in children. This study aimed to investigate the association between serum concentrations of vitamin E and AR to determine if the vitamin E level is correlated with the occurrence and severity of AR.

Methods: A total of 113 children were enrolled in this cross-sectional study. Sixty-five children in the outpatient group were diagnosed with AR, and 48 healthy children were recruited as controls. All subjects underwent serum vitamin E (adjusted for total cholesterol and triglycerides) measurements. Serum to total IgE (tIgE), the five most common allergen-specific IgE (sIgE) levels and skin prick test (SPT) were measured in children with AR. The severity of AR was assessed with the nasal symptoms score, and the situation of exposure to passive smoking were inquired.

Results: Serum vitamin E levels were significantly lower in the AR group than in the normal children (P < 0.001). A significant negative correlation was observed between serum vitamin E levels and sIgE as well as the SPT grade. Serum vitamin E levels were also inversely related to the nasal symptoms score; however, statistical significance was not found.

Conclusions: A significantly lower vitamin E level was found in children with AR. Lower serum vitamin E levels may have correlation with the occurrence of AR in children. However, serum vitamin E levels were not statistically correlated with the severity of AR.

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In vivo respiratory toxicology of cooking oil fumes: Evidence, mechanisms and prevention

Yongsheng Ma, Linjing Deng, Ping Ma, Yang Wu, Xu Yang, Fang Xiao, Qihong Deng

J Hazard Mater . 2020 Jul 12;402:123455. doi: 10.1016/j.jhazmat.2020.123455. Online ahead of print.

Abstract

Background: As cooking is an essential part of people’s daily life, cooking oil fumes (COF) has been recognized as one of the major indoor air pollutant. Mounting epidemiological evidence has indicated that COF exposure is significantly associated with an increased risk of various health effects including lung cancer, but toxicological studies are very limited.

Objectives: We conduct a systematic study to provide toxicological evidence of COF exposure on the lungs, to examine the underlying toxicological mechanism, and to suggest intervention measures to mitigate this toxicity.

Methods: A total 96 female rats were randomly divided into control groups, COF exposure groups (0.2, 2, 20 mg/kg) and vitamin E protection groups, receiving appropriate treatment for 30 days. First we measured airway hyperresponsiveness (AHR) followed by a lung histological analysis to investigate the toxicological effects of COF. We next analyzed the biomarkers of oxidative stress, inflammation, and apoptosis to examine the underlying toxicological mechanism, and finally we investigated the protective effects of vitamin E against the toxicity of COF.

Results: AHR measurement indicated that the airway resistance increased with the COF dose and the lung histological assay showed narrowing of the airway lumen, which provided evidence of the toxicological effects of COF. The biomarkers of oxidative stress (ROS and MDA), pro-inflammation (TNF-α and IL-1β), and apoptosis (NF-κB and Caspase-3) were all significantly increased with COF dose. We observed that above toxicological effects and biomarker levels induced by COF were significantly ameliorated after administration of VE.

Conclusion: The toxicity of cooking oil fumes on the lungs is clear from the evidence and mechanism, and can be ameliorated by vitamin E. We suggested that oxidative stress may be primarily responsible for the observed cooking oil fumes-induced toxicity.

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Impact of vitamins A, B, C, D, and E supplementation on improvement and mortality rate in ICU patients with coronavirus-19: a structured summary of a study protocol for a randomized controlled trial

Mohammad Taghi Beigmohammadi, Sama Bitarafan, Azin Hoseindokht, Alireza Abdollahi, Laya Amoozadeh, Maedeh Mahmoodi Ali Abadi, Morteza Foroumandi

Trials . 2020 Jul 6;21(1):614. doi: 10.1186/s13063-020-04547-0.

Abstract

Objectives: This study will evaluate the main hypothesis that supplementation with vitamins A, B, C, D, and E significantly improves the severity and mortality rate in ICU patients with COVID-19.

Trial design: This study is a randomized, single-blinded, two-arm (1:1 ratio) parallel group clinical trial.

Participants: We are conducting this study in patients with COVID-19 admitted to intensive care units at the Imam Khomeini Hospital Complex in Tehran, Iran. The inclusion criteria are as follows: (1) aged between 20 and 60 years, (2) both male and female patients with COVID-19, (3) clinical or definitive diagnosis (using polymerase chain reaction (PCR) test), (4) patients have not participated in other clinical trials, and (5) no renal or hepatic abnormalities. The exclusion criteria are as follows: (1) patients with specific and rare viral diseases such as HIV and (2) patients who have been undergoing chemotherapy for the past month.

Intervention and comparator: Duration of intervention: 7 days from randomization Intervention in the treatment group: Vitamin A 25,000 IU daily Vitamin D 600,000 IU once during study Vitamin E 300 IU twice daily Vitamin C is taken four times per day B vitamins are taken as a daily Soluvit [which included thiamine nitrate 3.1 mg, sodium riboflavin phosphate 4.9 mg (corresponding to vitamin B2 3.6 mg), nicotinamide 40 mg, pyridoxine hydrochloride 4.9 mg (corresponding to vitamin B6 4.0 mg), sodium pantothenate 16.5 mg (corresponding to pantothenic acid 15 mg), sodium ascorbate 113 mg (corresponding to vitamin C 100 mg), biotin 60 μg, folic acid 400 μg, and cyanocobalamin 5 μg] The control group will not receive any supplements or placebo. All supplements are made in Iran except for Soluvit (from Fresenius Kabi, New Zealand).

Main outcomes: 1. Weight, height, and BMI 2. Severity of pulmonary involvement according to CT scan 3. Respiratory support (invasive or non-invasive) 4. Percentage of oxygen saturation (SpO2 level) 5. Serum levels of WBC, CRP, ESR, IL6, IFN-G, and TNF-α 6. The patient’s body temperature 7. The presence or absence of involvement of organs other than the lungs (e.g., heart, liver, kidneys) 8. Duration of hospitalization 9. Mortality rate RANDOMIZATION: At baseline, eligible patients were randomly assigned to a 1:1 ratio to one of two groups: intervention and control. Block randomization is used based on the gender of patients.

Blinding (masking): Patients are unaware of being placed in the intervention or control groups after signing consent. All treatment staff will be aware of which group each of the patients is in due to the specific conditions of the ICU and the absence of placebo for the control group.

Numbers to be randomized (sample size): The researchers plan to include 60 patients in total, with 30 patients in each group.

Trial status: This is the first version of the protocol which started on April 2, 2020. Recruitment began April 2, 2020, and is expected to be complete by July 4, 2020.

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Vitamin E promotes ovine Sertoli cell proliferation by regulation of genes associated with cell division and the cell cycle

Yuefeng Gao, Wei Lu, Luyang Jian, Zoltan Machaty, Hailing Luo

Anim Biotechnol . 2020 Jul 2;1-9. doi: 10.1080/10495398.2020.1788044. Online ahead of print.

Abstract

The effect of Vitamin E on the proliferation of ovine Sertoli cells was investigated. Sertoli cells were isolated and treated with various amounts of Vitamin E (0 μM, 400 μM, 800 μM, 1000 μM, 1200 μM, 1400 μM and 1600 μM) for 24 h. We found that at the concentration of 1200 μM, Vitamin E promoted Sertoli cell proliferation very effectively. It also increased the proportion of cells in the G1 phase while reduced that in the S and G2/M phases, suggesting that its effect on Sertoli cell proliferation is achieved by enhancing progression through the cell cycle. In addition, Vitamin E significantly up-regulated the transcript level of the PDPN, BMP6, AMPKα, GSK3β, Myc, and CDK6 genes and down-regulated that of PPARγ, Cyclin B1 and CDK4 as determined by qRT-PCR. Western blot analysis revealed that the expression of BMP6 and PDPN was also upregulated at the protein level, in accordance with the results of the qRT-PCR. Taken together, Vitamin E promoted Sertoli cell proliferation by affecting the expression of genes that regulate cell division and the cell cycle; this indicates that it can have a positive effect on sheep reproductive performance.

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Culprit or Correlate? An Application of the Bradford Hill Criteria to Vitamin E Acetate

Ryan Feldman, Jonathan Meiman, Matthew Stanton, David D Gummin

Arch Toxicol . 2020 Jun;94(6):2249-2254. doi: 10.1007/s00204-020-02770-x. Epub 2020 May 25.

Abstract

Vitamin E acetate (VEA) has come under significant scrutiny due to its association with e-cigarette, or vaping, product use-associated lung injury (EVALI). In 1965, Sir Austin Bradford Hill proposed a set of criteria used to critically assess an association for causality. In this article, we apply the Bradford Hill causation criteria to VEA and the EVALI outbreak to clarify what further areas of study are needed to strengthen the causal argument. Additionally, we highlight the need for systematized approaches to rapidly identify the cause of mass poisoning events of unknown etiology.

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