Less widespread plant oils as a good source of vitamin E

Trela A, Szymańska R

Food Chem. 2019 Oct 30;296:160-166. doi: 10.1016/j.foodchem.2019.05.185. Epub 2019 May 28.

Abstract

Vitamin E is a family of related compounds with different vitamin E activities and antioxidant properties that includes tocopherols, tocotrienols and plastochromanol-8. Plant oils could serve as an industrial source not only of tocopherols, but also tocotrienols and plastochromanol-8, which exhibit much stronger antioxidant activities than tocopherols. The aim of this study was a quantitative and qualitative analysis of vitamin E in certain plant oils. We demonstrated the presence of vitamin E derivatives in all the plant oils tested. The highest tocopherol contents were in pomegranate, wheat germ and raspberry seed oils. In general, γ-tocopherol was the predominant tocopherol homologue. Tocotrienols were also identified in most of the oils, but their content was much lower. The highest concentration of tocotrienols was in coriander seed oil. Plastochromanol-8 was present in most of the oils, but wheat germ oil was the richest source.

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Vitamin E supplementation ameliorates the hepatotoxicity induced by Tramadol: toxicological, histological and immunohistochemical study

Ibrahim MA, Ibrahim HM, Mohamed AA, Tammam HG

Toxicol Mech Methods. 2019 Oct 29:1-12. doi: 10.1080/15376516.2019.1681043.

Abstract

Several deleterious effects of Tramadol including deaths were reported especially when used in large doses. Being metabolized mainly in the liver, Tramadol have serious hepatotoxic effects. This study investigates the effect of vitamin E on Tramadol-induced hepatotoxicity in rats by evaluating the antioxidant biochemical markers, the histopathological and immunohistochemical changes.Thirty adult mature male albino rats were divided into five groups (Gs); G1: negative control; G2: received Tramadol 150 mg/kg, G 3-5: received Tramadol plus vitamin E in concentrations of 50 mg/kg, 100 mg/kg and 200 mg/kg respectively. Liver function parameters and oxidative markers in liver tissue (CAT, SOD, GSH, and MDA) were estimated. Liver samples were processed for histopathological and immunohistochemical (Caspase 3 and TNF[Formula: see text]) examinations. The results indicated that Sub-chronic administration of Tramadol resulted in impaired liver functions, increased oxidative stress parameters with decreased antioxidant capacity of liver tissues, severe hepatocellular damage (hydropic degeneration, steatosis and apoptosis) and strong immunoexpression to TNF[Formula: see text] and Caspase 3. All these effects were ameliorated with concomitant administration of vitamin E especially with high doses. The co-treatment of Tramadol-intoxicated rats with Vitamin E, especially in high doses, protects against hepatic toxicity.

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Vitamin E but Not GSH Decreases Reactive Oxygen Species Accumulation and Enhances Sperm Production during In Vitro Maturation of Frozen-Thawed Prepubertal Mouse Testicular Tissue

Arkoun B, Galas L, Dumont L, Rives A, Saulnier J, Delessard M, Rondanino C, Rives N

Int J Mol Sci. 2019 Oct 29;20(21). pii: E5380. doi: 10.3390/ijms20215380.

Abstract

Freezing-thawing procedures and in vitro culture conditions are considered as a source of stress associated with increased reactive oxygen species (ROS) generation, leading to a damaged cell aerobic metabolism and consequently to oxidative stress. In the present study, we sought to investigate whether vitamin E (Vit E) or reduced glutathione (GSH) enhances sperm production by decreasing ROS accumulation during in vitro maturation of prepubertal mice testes. Testes of prepubertal mice were cryopreserved using a freezing medium supplemented or not supplemented with Vit E and were cultured after thawing. In presence of Rol alone in culture medium, frozen-thawed (F-T) testicular tissues exhibited a higher ROS accumulation than fresh tissue during in vitro culture. However, Vit E supplementation in freezing, thawing, and culture media significantly decreased cytoplasmic ROS accumulation in F-T testicular tissue during in vitro maturation when compared with F-T testicular tissue cultured in the presence of Rol alone, whereas GSH supplementation in culture medium significantly increased ROS accumulation associated with cytolysis and tissue disintegration. Vit E but not GSH promoted a better in vitro sperm production and was a suitable ROS scavenger and effective molecule to improve the yield of in vitro spermatogenesis from F-T prepubertal mice testes. The prevention of oxidative stress in the cytoplasmic compartment should be regarded as a potential strategy for improving testicular tissue viability and functionality during the freeze-thaw procedure and in vitro maturation.

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Gamma-tocopherol ameliorates hyperglycemia-induced hepatic inflammation associated with NLRP3 inflammasome in alloxan-induced diabetic mice

Lee H, Lim Y

Nutr Res Pract. 2019 Oct;13(5):377-383. doi: 10.4162/nrp.2019.13.5.377.

Abstract

BACKGROUND/OBJECTIVES:

Hyperglycemia-induced hepatic damage has been recognized as one of the major cause of complications in diabetes. Hepatic complications are associated with inflammation and oxidative stress in diabetes. In this study, we investigated the hypothesis that gamma-tocopherol (GT) supplementation ameliorates NLRP3 inflammasome associated hepatic inflammation in diabetes.

MATERIALS/METHODS:

Diabetes was induced by the intraperitoneal injection of alloxan (150 mg/kg. BW) in ICR mice. All mice were fed with a control diet (AIN-76A). After diabetes was induced (fasting glucose level ≥ 250 mg/dL), the mice were treated with tocopherol-stripped corn oil or GT-supplemented (35 mg/kg) corn oil, respectively, by gavage for 2 weeks.

RESULTS:

GT supplementation reduced fasting blood glucose levels in diabetic mice relative to non-treated diabetic mice. Moreover, GT supplementation ameliorated hyperglycemia-induced hepatic damage by regulation of NOD-like receptor protein 3 (NLRP3)-inflammasome associated inflammation represented by NLRP3, apoptosis-associated speck-like protein containing a caspase-recruitment domain, caspase-1, nuclear factor-κB pathway as well as oxidative stress demonstrated by nuclear factor erythroid 2-related factor 2, NAD(P)H dehydrogenase quinone 1, catalase and glutathione-dependent peroxidase in diabetic mice.

CONCLUSION:

The findings suggested that GT supplementation ameliorated hepatic damage by attenuating inflammation and oxidative stress in alloxan-induced diabetic mice. Taken together, GT could be a beneficial nutrient that can ameliorate inflammatory responses associated with NLRP3 inflammasome in hyperglycemia-induced hepatic damage.

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A meta-analysis of peripheral tocopherol levels in age-related cognitive decline and Alzheimer’s disease

Ashley S, Bradburn S, Murgatroyd C

Nutr Neurosci. 2019 Oct 29:1-15. doi: 10.1080/1028415X.2019.1681066

Abstract

Objectives: Findings from observational studies and clinical trials on the associations between vitamin E and dementia remain controversial. Here we conducted a meta-analysis to determine the difference in blood tocopherols levels between patients with Alzheimer’s disease (AD) or age-related poor cognitive function and healthy controls.Methods: Standardised mean difference (SMD) and 95% confidence intervals (CIs) were calculated and entered into a random effects model. Study quality, heterogeneity and publication bias were also investigated.Results: Thirty-one articles were included in the meta-analysis, which included analyses for α-, β-, γ– and δtocopherols. These results indicated that individuals with AD or age-related cognitive deficits and mild cognitive impairment (MCI) had lower circulatory concentrations of α-tocophenol compared with healthy controls (AD: SMD = -0.97, 95% confidence interval [CI] = -1.27 to -0.68, Z = 6.45, P < 0.00001; age-related cognitive deficits and MCI: SMD = -0.72, 95% CI = -1.12 to -0.32, Z = -3., P < 0.0005). Levels of β-, γ– and δ-tocophenols did not significantly differ between groups of AD and age-related cognitive deficits compared to controls.Discussion: These results suggest that lower αtocopherol levels have a strong association with AD and MCI supporting evidence for the role of diet and vitamin E in AD risk and age-related cognitive decline.

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Vitamin E preconditioning alleviates in vitro thermal stress in cultured human epidermal keratinocytes

Butt H, Mehmood A, Ali M, Tasneem S, Tarar MN, Riazuddin S

Life Sci. 2019 Oct 22;239:116972. doi: 10.1016/j.lfs.2019.116972.

Abstract

AIMS:

Thermal burns are the most common type of skin injuries. Clinically, the deteriorating thermal wounds have been successfully treated with skin cell sheets, suspensions or bioengineered skin substitutes. After thermal injury, oxidative microenvironment prevalent in the burnt tissue due to imbalance between production of free radicals and antioxidants defense aiding to destruction of cellular or tissue components. However, depleted antioxidant content particularly vitamin E after heat injury challenges efficient regenerative and healing capacity of transplanted cells. Thus, aim of current study was to pretreat human epidermal keratinocytes with vitamin E in order to enhance their survival rate and therapeutic ability under oxidative microenvironment induced by in vitro heat stress.

MAIN METHODS:

Keratinocytes were treated with 100 μM vitamin E at 37 °C for 24 h followed by thermal stress at 51 °C for 10 min. Cell viability and cytotoxicity assays, gene expression analysis and paracrine release analysis were performed.

KEY FINDINGS:

Vitamin E preconditioning resulted in significantly improved cell morphology, enhanced viability and reduced lactate dehydrogenase release. Furthermore, Vitamin E preconditioned cells exposed to thermal stress showed significant down-regulated expression of BAX and up-regulated expression of PCNA, BCL-XL, vascular endothelial growth factor (VEGF), involucrin, transglutaminase 1 (TGM1) and filaggrin (FLG) escorted by increased paracrine release of VEGF, basic fibroblast growth factor (bFGF) and epidermal growth factor (EGF).

SIGNIFICANCE:

Results of the current study suggest that clinical transplantation of vitamin E preconditioned keratinocytes alone or in combination with dermal fibroblasts in skin substitutes for the treatment of thermally injured skin.

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Oxidative Stress Mediates Anxiety-Like Behavior Induced by High Caffeine Intake in Zebrafish: Protective Effect of Alpha-Tocopherol

de Carvalho TS, Cardoso PB, Santos-Silva M, Lima-Bastos S, Luz WL, Assad N, Kauffmann N, Passos A, Brasil A, Bahia CP, Moraes S, Gouveia A Jr, de Jesus Oliveira Batista E, Oliveira KRMH, Herculano AM

Oxid Med Cell Longev. 2019 Oct 21;2019:8419810. doi: 10.1155/2019/8419810

Abstract

Anxiety is a common symptom associated with high caffeine intake. Although the neurochemical mechanisms of caffeine-induced anxiety remain unclear, there are some evidences suggesting participation of oxidative stress. Based on these evidences, the current study is aimed at evaluating the possible protective effect of alpha-tocopherol (TPH) against anxiety-like behavior induced by caffeine (CAF) in zebrafish. Adult animals were treated with CAF (100 mg/kg) or TPH (1 mg/kg)+CAF before behavioral and biochemical evaluations. Oxidative stress in the zebrafish brain was evaluated by a lipid peroxidation assay, and anxiety-like behavior was monitored using light/dark preference and novel tank diving test. Caffeine treatment evoked significant elevation of brain MDA levels in the zebrafish brain, and TPH treatment prevented this increase. Caffeine treatment also induced anxiety-like behavior, while this effect was not observed in the TPH+CAF group. Taken together, the current study suggests that TPH treatment is able to inhibit oxidative stress and anxiety-like behavior evoked by caffeine.

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Vitamins D and E Stimulate the PI3K-AKT Signalling Pathway in Insulin-Resistant SK-N-SH Neuronal Cells

Zaulkffali AS, Md Razip NN, Syed Alwi SS, Abd Jalil A, Abd Mutalib MS, Gopalsamy B, Chang SK, Zainal Z, Ibrahim NN, Zakaria ZA, Khaza'ai H

Nutrients. 2019 Oct 19;11(10). pii: E2525. doi: 10.3390/nu11102525.

Abstract

This study investigated the effects of vitamins D and E on an insulin-resistant model and hypothesized that this treatment would reverse the effects of Alzheimer’s disease (AD) and improves insulin signalling. An insulin-resistant model was induced in SK-N-SH neuronal cells with a treatment of 250 nM insulin and re-challenged with 100 nM at two different incubation time (16 h and 24 h). The effects of vitamin D (10 and 20 ng/mL), vitamin E in the form of tocotrienol-rich fraction (TRF) (200 ng/mL) and the combination of vitamins D and E on insulin signalling markers (IRPI3KGLUT3GLUT4, and p-AKT), glucose uptake and AD markers (GSK3β and TAU) were determined using quantitative real-time polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA). The results demonstrated an improvement of the insulin signalling pathway upon treatment with vitamin D alone, with significant increases in IRPI3KGLUT3GLUT4 expression levels, as well as AKT phosphorylation and glucose uptake, while GSK3β and TAU expression levels was decreased significantly. On the contrary, vitamin E alone, increased pAKT, reduced the ROS as well as GSK3β and TAU but had no effect on the insulin signalling expression levels. The combination of vitamins D and E only showed significant increase in GLUT4p-AKT, reduced ROS as well as GSK3β and TAU. Thus, the universal role of vitamin D, E alone and in combinations could be the potential nutritional agents in restoring the sensitivity of neuronal cells towards insulin and delaying the pathophysiological progression of AD.

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Vitamin E is an effective treatment for nonalcoholic steatohepatitis in HIV mono-infected patients

Sebastiani G, Saeed S, Lebouche B, de Pokomandy A, Szabo J, Haraoui LP, Routy JP, Wong P, Deschenes M, Ghali P, Klein M; LIVEHIV Study Group.

AIDS. 2019 Oct 16. doi: 10.1097/QAD.0000000000002412.

Abstract

OBJECTIVE:

Human immunodeficiency virus (HIV)-infected patients are at increased risk of nonalcoholic steatohepatitis (NASH). Vitamin E is recommended for treatment of NASH in the general population. However, its safety and efficacy among HIV-infected patients remain unknown.

DESIGN:

Single centre, phase IV, open-label, single arm clinical trial.

METHODS:

HIV mono-infected patients without significant alcohol intake or viral hepatitis coinfection were included. The diagnosis of NASH was based on the co-existence of fatty liver, diagnosed by controlled attenuation parameter (CAP) ≥ 248 dB/m, and significant hepatocyte apoptosis, defined by the serum biomarker cytokeratin 18 (CK-18) >130.5 U/L. Participants were treated with 800 IU daily of oral vitamin E (alpha-tocopherol) for 24 weeks, and followed for an additional 24 weeks post-discontinuation. Generalized linear mixed effects models were used to evaluate changes in ALT, CAP and CK-18 at the completion of treatment and end of follow-up, controlling for pre-treatment trends.

RESULTS:

A total of 27 patients were included. Four (15%) had a pretreatment liver biopsy, which confirmed the diagnosis of NASH in all cases. Compared to baseline, 24 weeks of vitamin E treatment improved ALT (-27 units/L; 95% confidence interval [CI] -37, –17), CAP scores (-22 dB/m; 95% CI -42, -1) and CK-18 (-123 units/L; 95% CI -201, -46). Conversely, there was no change in BMI. No serious adverse event was reported and no patient was lost to follow-up.

CONCLUSION:

In this first clinical trial, we showed that vitamin E is an effective and well-tolerated treatment for NASH in HIV-infected patients.

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Vitamin E protects against monosodium glutamate-induced acute liver injury and hepatocyte ultrastructural alterations in rats

Eid RA, Al-Shraim M, Zaki MS, Kamar SS, Abdel Latif NS, Negm S, Al-Ani B, Haidara MA

Ultrastruct Pathol. 2019;43(4-5):199-208. doi: 10.1080/01913123.2019.1673860.

Abstract

Food additives such as nitrates and nitrites, and monosodium glutamate (MSG) used in the food industry increase the risk of certain cancers and inflict damage to vital organs. We sought to determine whether the antioxidant vitamin E can protect against liver injuries induced by a toxic dose of MSG in a rat model of MSG-induced acute liver injury. The model group of rats received a daily dose of MSG (4 gm/kg) for 7 days, whereas the protective groups were either received a 100 mg/kg vitamin E plus MSG or 300 mg/kg vitamin E plus MSG for 7 days. Rats were then sacrificed at day 8. Transmission and light microscopy images revealed substantial liver tissue damage induced by MSG in the model group as demonstrated by apoptotic hepatocytes with Pyknotic nuclei and irregular nuclear membrane, and cytoplasm displayed many vacuoles, swollen mitochondria, dilated endoplasmic reticulum, dilated blood sinusoids and bundles of collagen fibers in extracellular space. Treatment of the model group with vitamin E showed a substantial protection of liver tissue and hepatocellular architecture by 300 mg/kg vitamin E compared to a partial protection by 100 mg/kg vitamin E. In addition, MSG significantly (p < .05) modulated serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), superoxide dismutase (SOD), and glutathione peroxidase (GPx), which were significantly (p < .05) protected with vitamin E. Thus, vitamin E at 300 mg/kg effectively protects against MSG-induced acute liver injury in rats, possibly via the inhibition of inflammation, and up-regulation of endogenous antioxidants.

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