Maternal supplementation with a megadose of vitamin A reduces colostrum level of α-tocopherol: a randomised controlled trial.

Grilo EC, Medeiros WF, Silva AG, Gurgel CS, Ramalho HM, Dimenstein R.

J Hum Nutr Diet. 2016 Oct;29(5):652-61. doi: 10.1111/jhn.12381.

Abstract

Maternal supplementation with vitamin A is one of the strategies for controlling its deficiency in the mother-child dyad, although studies with animals showed that supplementation with high doses of vitamin A reduces the levels of α-tocopherol (vitamin E) in the mother’s serum and milk. The objective of the present study was to assess the influence of maternal supplementation with vitamin A on the concentration of retinol and α-tocopherol in human milk. From the results obtained, we concluded that maternal supplementation with high doses of vitamin A increased the colostrum level of this nutrient but reduced the bioavailability of α-tocopherol, which may harm the newborn’s health because newborns have limited vitamin E reserves.

Cook-Mills J, Gebretsadik T, Abdala-Valencia H, Green J, Larkin EK, Dupont WD, Shu XO, Gross M, Bai C, Gao YT, Hartman TJ, Rosas-Salazar C, Hartert T.

Thorax. 2016 Oct;71(10):954-6. doi: 10.1136/thoraxjnl-2016-208494.

Abstract

Prospective epidemiological studies, observational cross-sectional studies and some randomised prevention trials have demonstrated inconsistent findings of the impact of vitamin E on asthma risk. The goals of this study were to explore whether this differing association of vitamin E on asthma risk is due to an interaction of vitamin E isoforms. To address this question, in a population-based asthma incidence study we assessed the interaction between the plasma concentrations of vitamin E isoforms α-tocopherol and γ-tocopherol on asthma risk. Second, to understand the mechanisms of any interaction of these isoforms, we conducted experimental supplementation of α-tocopherol and γ-tocopherol isoforms in mice on the outcome of allergic airway inflammation. We found that in the highest γ-tocopherol tertile, low levels of α-tocopherol were associated with increased asthma risk, while highest tertile α-tocopherol levels trended to be protective. Similarly, in a mouse model of asthma, diet supplementation with α-tocopherol decreased lung inflammation in response to house dust mite (HDM) challenge. In contrast, diet supplementation with γ-tocopherol increased lung inflammation in response to HDM. These human and animal studies provide evidence for the competing effects of the vitamin Eisoforms, in physiological concentrations, on asthma and allergic airway disease.

Shahidi F, de Camargo AC.

Int J Mol Sci. 2016 Oct 20;17(10). pii: E1745. Review.

Abstract

Edible oils are the major natural dietary sources of tocopherols and tocotrienols, collectively known as tocols. Plant foods with low lipid content usually have negligible quantities of tocols. However, seeds and other plant food processing by-products may serve as alternative sources of edible oils with considerable contents of tocopherols and tocotrienols. Tocopherols are among the most important lipid-soluble antioxidants in food as well as in human and animal tissues. Tocopherols are found in lipid-rich regions of cells (e.g., mitochondrial membranes), fat depots, and lipoproteins such as low-density lipoprotein cholesterol. Their health benefits may also be explained by regulation of gene expression, signal transduction, and modulation of cell functions. Potential health benefits of tocols include prevention of certain types of cancer, heart disease, and other chronic ailments. Although deficiencies of tocopherol are uncommon, a continuous intake from common and novel dietary sources of tocopherols and tocotrienols is advantageous. Thus, this contribution will focus on the relevant literature on common and emerging edible oils as a source of tocols. Potential application and health effects as well as the impact of new cultivars as sources of edible oils and their processing discards are presented. Future trends and drawbacks are also briefly covered.

Zainuddin A, Chua KH, Tan JK, Jaafar F, Makpol S.

J Physiol Biochem. 2016 Oct 14. [Epub ahead of print]

Abstract

Human diploid fibroblasts (HDFs) proliferation in culture has been used as a model of aging at the cellular level. Growth arrest is one of the most important mechanisms responsible for replicative senescence. Recent researches have been focusing on the function of vitamin E in modulating cellular signaling and gene expression. Therefore, the aim of this study was to elucidate the effect of palm γ-tocotrienol (vitamin E) in modulating cellular aging through p16^INK4a pathway in HDF cells. Primary culture of senescent HDFs was incubated with 70 μM of palm γ-tocotrienol for 24 hours. Silencing of p16^INK4a was carried out by siRNA transfection. RNA was extracted from the different treatment groups and gene expression analysis was carried out by real-time reverse transcription polymerase chain reaction. Proteins that were regulated by p16^INK4a were determined by western blot technique. The finding of this study showed that p16^INK4a mRNA was overexpressed in senescent HDFs, and hypophosphorylated-pRb and cyclin D1 protein expressions were increased (p < 0.05). However, downregulation of p16^INK4a and hypophosphorylated-pRb and cyclin D1 protein expressions (p < 0.05) by γ-tocotrienol led to modulation of the cell cycle regulation during cellular aging. In conclusion, senescent HDFs showed change in biological process specifically in cell cycle regulation with elevated expression of genes and proteins which may contribute to cell cycle arrest. Palm γ-tocotrienol may delay cellular senescence of HDFs by regulating cell cycle through downregulation of p16^INK4a and hypophosphorylated-pRb and cyclin D1 protein expressions.

Hemilä H.

Clin Interv Aging. 2016 Oct 3;11:1379-1385.

Abstract

Vitamin E has influenced the immune system in laboratory studies. Dozens of animal experiments have found that vitamin E offered protection against infections caused by viruses and bacteria. Previously, significant heterogeneity was found in the effect of vitamin E supplementation on pneumonia in humans. The aim of this study was to examine how the effect of vitamin E on pneumonia risk depends on age. Although the evidence of benefit from vitamin E against pneumonia in elderly males is strong in this analysis, the overall findings about vitamin E have been complex. Further research on vitamin E in nonsmoking elderly males is warranted.

Ourique GM, Saccol EM, Pês TS, Glanzner WG, Schiefelbein SH, Woehl VM, Baldisserotto B, Pavanato MA, Gonçalves PB, Barreto KP.

Food Chem Toxicol. 2016 Sep;95:159-67. doi: 10.1016/j.fct.2016.07.011.

Abstract

Long-term administration of valproic acid (VPA) is known to promote reproductive impairment mediated by increase in testicular oxidative stress. Vitamin E (VitE) is a lipophilic antioxidant known to be essential for mammalian spermatogenesis. However, the capacity of this vitamin to abrogate the VPA-mediated oxidative stress has not yet been assessed. In the current study, we evaluated the protective effect of VitE on functional abnormalities related to VPA-induced oxidative stress in the male reproductive system. VPA (400 mg kg(-1)) was administered by gavage and VitE (50 mg kg(-1)) intraperitoneally to male Wistar rats for 28 days. Analysis of spermatozoa from the cauda epididymides was performed. The testes and epididymides were collected for measurement of oxidative stress biomarkers. Treatment with VPA induced a decrease in sperm motility accompanied by an increase in oxidative damage to lipids and proteins, depletion of reduced glutathione and a decrease in total reactive antioxidant potential on testes and epididymides. Co-administration of VitE restored the antioxidant potential and prevented oxidative damage on testes and epididymides, restoring sperm motility. Thus, VitE protects the reproductive system from the VPA-induced damage, suggesting that it may be a useful compound to minimize the reproductive impairment in patients requiring long-term treatment with VPA.

Parnan Emamverdikhan A, Golmakani N, Tabassi SA, Hassanzadeh M, Sharifi N, Shakeri MT.

Iran J Nurs Midwifery Res. 2016 Sep-Oct;21(5):475-481.

Abstract

Menopause is associated with various complications such as depression, sleep disorders, and genitourinary atrophy. Vaginal atrophy occurs due to the loss of steroid hormones, and its major symptoms include vaginal dryness, itching, dyspareunia, and bleeding after intercourse. According to the literature, vitamin E plays a key role in estrogen stability. The aim of this study was to compare the effects of vitamin E suppositories and conjugated estrogen vaginal cream on vaginal atrophy.

In this clinical trial, 52 postmenopausal women, who were referred to a gynecology clinic in 2013, were recruited and randomly divided into two groups (26 cases per group). One group received 100 IU of vitamin E suppositories (n = 26), whereas the other group applied 0.5 g of conjugated estrogen cream for 12 weeks. Vaginal maturation value (VMV) was compared between the two groups before and after the intervention. VMV ≤ 55 was regarded as a cut-off point for vaginal atrophy. Treatment success was defined as a 10-unit increase in VMV, compared to the baseline value. Data were analyzed by Friedman test and Mann-Whitney test. P value less than 0.05 was considered statistically significant.

The mean VMV in the vitamin E group before the treatment and after 4, 8, and 12 weeks of treatment was 43.78 ± 13.75, 69.07 ± 22.75, 77.86 ± 21.79, and 80.59 ± 19.23, respectively. The corresponding values in the estrogen cream group were 42.86 ± 14.40, 86.98 ± 12.58, 92.65 ± 15, and 91.57 ± 14.10, respectively. VMV significantly improved in both the treatment groups after the intervention, compared to the preintervention period (P < 0.001). Treatment success was reported in both groups, although estrogen cream (100%) appeared to be more effective after 4 weeks of treatment, compared to vitamin E suppositories (76.9%) (P = 0.01). Based on the findings, use of vitamin E suppositories could improve the laboratory criteria for vaginal atrophy and treatment success. Therefore, vitamin E suppositories are suggested for relieving the symptoms of vaginal atrophy, especially in women who are unable to use hormone therapy or cope with the associated side effects.

Strait RT, Camargo CA.

Expert Rev Respir Med. 2016 Aug;10(8):881-90. doi: 10.1080/17476348.2016.1184090.

Abstract

Asthma, a heterogeneous disease with multiple phenotypes, remains a significant health problem. Present treatments are not curative and prevention should be our ultimate goal. Vitamin E supplementation presents a potential easy and cheap preventive therapy but the results of studies are confusing and sometimes contradictory. Clarification is needed.Animal studies and research in pregnant women suggest enhanced lifetime resistance to asthma with appropriate fetal exposure to vitamin E. Vitamin E‘s preventive role is complex and includes functional variations of the different isoforms. Expert commentary: We review the most recent literature on the role of vitamin E isoforms on: lung inflammation, immune development, animal and clinical studies during pregnancy, and the potential influence of vitamin E isoforms on asthma development in offspring. We point out where data are seemingly contradictory, explain why this is so, and comment on where further clarifying research is needed and its future direction.

Li Y, Bharath LP, Qian Y, Ruan T, Anandh Babu PV, Bruno RS, Symons JD, Jalili T.

Exp Biol Med (Maywood). 2016 Jul 27. pii: 1535370216661780. [Epub ahead of print]

Abstract

Endothelial dysfunction occurs when there are imbalances between factors that regulate the synthesis and degradation of nitric oxide (NO^•), and has been reported in patients with hyperglycemia and insulin resistance. We reported that supplementation with γ-tocopherol (γ-T) in humans limits impairments in endothelial function otherwise induced by postprandial hyperglycemia. Given the rapid metabolism of γ-T into γ-carboxyethyl hydroxychroman (γ-CEHC), we hypothesized that the vasoprotective activities of γ-T could be attributed to its metabolite γ-CEHC. To test this, human aortic endothelial cells (HAECs) treated with 0 (vehicle control) or 3 µM γ-CEHC for 24 h prior to incubation with normal (5 mM) or high (25 mM) glucose for 48 h. High-glucose increased levels of uncoupled endothelial nitric oxide synthase (eNOS) as evidenced by reduced (p < 0.05) eNOS dimer:monomer. High glucose also prevented insulin-stimulated increases in p-Akt^Ser473: total Akt, p-eNOS^Ser1177: total eNOS, and NO^• production. These adverse changes were accompanied by increased (p < 0.05) reactive oxygen species and mRNA expression of inflammatory mediators (VCAM-1, E-selectin, IL-8). However, each deleterious response evoked by high glucose was prevented when HAECs were incubated with γ-CEHC prior to the high glucose challenge. Taken together, our data support the hypothesis that vascular protection provided by γ-T in vivo may be elicited through the bioactivity of its metabolite, γ-CEHC. Furthermore, it is possible that the antioxidant and anti-inflammatory activities of γ-CEHC may mediate this protective activity.

Araoud M, Neffeti F, Douki W, Khaled L, Najjar MF, Kenani A, Houas Z.

Environ Toxicol. 2016 Jul;31(7):842-54. doi: 10.1002/tox.22095.

Abstract

The role of alpha-tocopherol on nephrotoxicity and hepatotoxicity induced by methamidophos (MT) was investigated in wistar rats. Animals were given via gavage, for four weeks, a low dose of MT (MT1), a high dose of MT (MT2), vitamin E (200 mg/kg of bw) or both MT2 plus vitamin E (Vit E) and control group was given distillate water. MT treatment resulted in a significant decrease in the body weight of MT2-treated group. Moreover, MT-treated groups had significantly lower butyrylcholinesterase (p < 0.01) and paraoxonase 1 (PON1) activities compared with the control group (p < 0.05). However, MT2-treated group had significantly higher alkaline phosphatase activity compared with untreated rats (p < 0.05). Both MT-treated groups had significantly higher urea (p < 0.01) and uric acid levels (p < 0.05) compared with the control group. However, significant low uric acid level (p < 0.05) was noted in MT2 plus vit E-treated rats compared with MT2-treated group. Histopathological changes in organ tissues were observed in both MT-treated groups and MT2 plus vit E-treated rats. However, the damage was reduced in MT2 plus vit E-treated rats. Therefore, this study deduces that alpha-tocopherol administration may ameliorate the adverse effects of subacute exposure to MT on rat liver and kidney and this antioxidant can protect PON1 from oxidative stress induced by this organophosphorus pesticide.