Can Low-Dose of Dietary Vitamin E Supplementation Reduce Exercise-Induced Muscle Damage and Oxidative Stress? A Meta-Analysis of Randomized Controlled Trials

Myunghee Kim, Hyeyoon Eo, Josephine Gahyun Lim, Hyunjung Lim, Yunsook Lim

Nutrients . 2022 Apr 12;14(8):1599. doi: 10.3390/nu14081599.

Abstract

Vitamin E plays an important role in attenuating muscle damage caused by oxidative stress and inflammation. Despites of beneficial effects from antioxidant supplementation, effects of antioxidants on exercise-induced muscle damage are still unclear. The aim of this meta-analysis was to investigate the effects of dietary vitamin E supplementation on exercise-induced muscle damage, oxidative stress, and inflammation in randomized controlled trials (RCTs). The literature search was conducted through PubMed, Medline, Science Direct, Scopus, SPORTDiscuss, EBSCO, Google Scholar database up to February 2022. A total of 44 RCTs were selected, quality was assessed according to the Cochrane collaboration risk of bias tool (CCRBT), and they were analyzed by Revman 5.3. Dietary vitamin E supplementation had a protective effect on muscle damage represented by creatine kinase (CK; SMD -1.00, 95% CI: -1.95, -0.06) and lactate dehydrogenase (SMD -1.80, 95% CI: -3.21, -0.39). Muscle damage was more reduced when CK was measured immediately after exercise (SMD -1.89, 95% CI: -3.39, -0.39) and subjects were athletes (SMD -5.15, 95% CI: -9.92, -0.39). Especially vitamin E supplementation lower than 500 IU had more beneficial effects on exercise-induced muscle damage as measured by CK (SMD -1.94, 95% CI: -2.99, -0.89). In conclusion, dietary vitamin E supplementation lower than 500 IU could prevent exercise-induced muscle damage and had greater impact on athletes.

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Effect of vitamin E supplementation on cardiometabolic risk factors, inflammatory and oxidative markers and hormonal functions in PCOS (polycystic ovary syndrome): a systematic review and meta-analysis

Ghazale Tefagh, Moloud Payab, Mostafa Qorbani, Farshad Sharifi, Yasaman Sharifi, Mahbubeh Sadat Ebrahimnegad Shirvani, Farzad Pourghazi, Rasha Atlasi, Zhaleh Shadman, Nafiseh Rezaei, Erfan Mohammadi-Vajari, Bagher Larijani, Mahbube Ebrahimpur

Sci Rep . 2022 Apr 6;12(1):5770. doi: 10.1038/s41598-022-09082-3.

Abstract

Polycystic ovary syndrome (PCOS) is a common endocrinopathy among reproductive-age women. Various therapeutical approaches are currently used to manage or control symptoms associated with PCOS. This systematic review intended to assess the effects of Vit E supplementation on cardiometabolic risk factors, inflammatory and oxidative markers, and hormonal functions in PCOS women based on the clinical trial’s results. The databases including PubMed, Scopus, Cochrane, Web of Science, and Embase were used to find all relevant studies. The authors reviewed all relevant clinical trials via systematic evaluation of abstracts and titles. Searches were conducted on August 1, 2020. After the initial search and reading of the article’s title and abstract, 353 articles were reviewed; finally, 12 articles met the inclusion criteria. Vitamin E supplementation improves lipid profile, decreases insulin and HOMA-IR levels. Furthermore, while Vitamin E supplementation decreases LH and testosterone concentrations, it increases FSH and progestrone concentrations. The following meta-analysis showed that vitamin E supplementation made statistically significant improvements in triglyceride (TG) and low-density lipoproteins (LDL) levels, meanwhile, pooled mean difference for waist circumference (WC) and HOMA-IR were also statistically significant. Supplementary regimens containing vitamin E can positively affect metabolic and hormonal parameters in women with PCOS.

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Fat Grafts Augmented With Vitamin E Improve Volume Retention and Radiation-Induced Fibrosis

Darren B Abbas, Christopher V Lavin, Evan J Fahy, Michelle Griffin, Nicholas J Guardino, Rahim S Nazerali, Dung H Nguyen, Arash Momeni, Michael T Longaker, Derrick C Wan

Aesthet Surg J . 2022 Mar 29;sjac066. doi: 10.1093/asj/sjac066. Online ahead of print.

Abstract

Background: Treatments for radiation-induced fibrosis range from vitamin E and pentoxifylline systemically to deferoxamine and fat grafting locally. Regarding fat grafting, volume retention hinders its long-term functionality and is affected by two factors: inflammation and necrosis secondary to hypovascularity.

Objective: We aimed to simultaneously improve fat graft retention and radiation-induced fibrosis by integrating vitamin E and pentoxifylline into fat grafts locally.

Methods: Forty adult CD-1 nude male mice at 6 weeks of age underwent scalp irradiation and recovered for four weeks to allow for the development of fibrosis. Mice received 200μL of donor human fat graft to the scalp. Mice were separated into 4 conditions: no grafting, fat graft without treatment, graft treated with pentoxifylline, and graft treated with vitamin E. Fat graft volume retention was monitored in-vivo using microCT scans at weeks 0, 1, 2, 4, 6, and 8 after grafting. Histological and cytokine analysis of the scalp skin and fat grafts were also performed.

Results: Vitamin E (VE) treated grafts had significant improvement in dermal thickness and collagen density of overlying skin compared to all other groups. VE decreased 8-isoprostane and increased CD31 + staining compared to the other grafted groups. Cytokine analysis revealed decreased inflammatory and increased angiogenic markers in both the fat graft and overlying skin of the vitamin E group. Fat graft volume retention was significantly improved in the vitamin E group starting at 1 week post grafting.

Conclusion: Radiation-induced fibrosis and fat graft volume retention are both simultaneously improved with local administration of vitamin E.

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Effect of tocotrienol on the primary progression of nonalcoholic steatohepatitis in a mouse model

Jun Noichi, Tomoko Ishiakawa, Ikuyo Ichi, Yoko Fujiwara

J Clin Biochem Nutr . 2022 Mar;70(2):140-146. doi: 10.3164/jcbn.21-69. Epub 2021 Oct 2.

Abstract

Tocotrienol (T3), a vitamin E (Vit E) isoform, is known to have both biological and antioxidant effects. Although alpha-tocopherol (α-Toc), another isoform of Vit E is suggested to be a useful treatment against nonalcoholic steatohepatitis (NASH), the effect of T3 on NASH is unclear. This study aimed to comparatively evaluate the effects of T3 and α-Toc on NASH in the early stage of NASH progression, using a recently established NASH mouse model induced by a choline-deficient l-amino acid-defined high-fat diet (CDAHFD). Six-week-old male mice were divided into four groups (n = 6 per group) and fed the CDAHFD for 1 week. The first group was given no other treatment (Pre). The other three groups continued the CDAHFD plus daily oral administration of Vit E-free corn oil (Control), corn oil containing α-Toc, or corn oil containing T3 for additional 2 weeks. Neither Vit E treatment changed the histologic features of NASH, but T3 significantly reduced the mRNA expression of several genes related to inflammation and fibrosis and α-Toc did not. These results suggested that oral T3 treatment was more effective than α-Toc at suppressing hepatic inflammation and fibrosis in the early stage of NASH progression in CDAHFD model mice.

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Potential of the Compounds from Bixa orellana Purified Annatto Oil and Its Granules (Chronic ®) against Dyslipidemia and Inflammatory Diseases: In Silico Studies with Geranylgeraniol and Tocotrienols

Mateus Alves Batista, Abrahão Victor Tavares de Lima Teixeira Dos Santos, Aline Lopes do Nascimento, Luiz Fernando Moreira, Indira Ramos Senna Souza, Heitor Ribeiro da Silva, Arlindo César Matias Pereira, Lorane Izabel da Silva Hage-Melim, José Carlos Tavares Carvalho

Molecules . 2022 Feb 28;27(5):1584. doi: 10.3390/molecules27051584.

Abstract

Some significant compounds present in annatto are geranylgeraniol and tocotrienols. These compounds have beneficial effects against hyperlipidemia and chronic diseases, where oxidative stress and inflammation are present, but the exact mechanism of action of such activities is still a subject of research. This study aimed to evaluate possible mechanisms of action that could be underlying the activities of these molecules. For this, in silico approaches such as ligand topology (PASS and SEA servers) and molecular docking with the software GOLD were used. Additionally, we screened some pharmacokinetic and toxicological parameters using the servers PreADMET, SwissADME, and ProTox-II. The results corroborate the antidyslipidemia and anti-inflammatory activities of geranylgeraniol and tocotrienols. Notably, some new mechanisms of action were predicted to be potentially underlying the activities of these compounds, including inhibition of squalene monooxygenase, lanosterol synthase, and phospholipase A2. These results give new insight into new mechanisms of action involved in these molecules from annatto and Chronic®.

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Tocotrienol in Pre-Eclampsia Prevention: A Mechanistic Analysis in Relation to the Pathophysiological Framework

Zaleha Abdullah Mahdy, Kok-Yong Chin, Nik Lah Nik-Ahmad-Zuky, Aida Kalok, Rahana Abdul Rahman

Cells . 2022 Feb 10;11(4):614. doi: 10.3390/cells11040614.

Abstract

The pathophysiology of pre-eclampsia involves two major pathways, namely systemic oxidative stress and subsequent generalised inflammatory response, which eventually culminates in endothelial cell injury and the syndrome of pre-eclampsia with multi-organ dysfunction. Aspirin has been used to reduce the risk of pre-eclampsia, but it only possesses anti-inflammatory properties without any antioxidant effect. Hence, it can only partially alleviate the problem. Tocotrienols are a unique form of vitamin E with strong antioxidant and anti-inflammatory properties that can be exploited as a preventive agent for pre-eclampsia. Many preclinical models showed that tocotrienol can also prevent hypertension and ischaemic/reperfusion injury, which are the two main features in pre-eclampsia. This review explores the mechanism of action of tocotrienol in relation to the pathophysiology of pre-eclampsia. In conclusion, the study provides sufficient justification for the establishment of a large clinical trial to thoroughly assess the capability of tocotrienol in preventing pre-eclampsia.

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Effect of α-tocopherol in alleviating the lipopolysaccharide-induced acute lung injury via inhibiting nuclear factor kappa-B signaling pathways

Mu Hu, Jielai Yang, Yang Xu

Bioengineered . 2022 Feb;13(2):3958-3968. doi: 10.1080/21655979.2022.2031399.

Abstract

Acute respiratory distress syndrome (ARDS) leads to the acute lung injury (ALI), a form of diffused alveolars injury, accompanied by severe inflammation and oxidative damage of alveolar epithelial cells. α-Tocopherol (α-TOH), one of the eight isoforms of vitamin E, is a natural antioxidant-free radical. We aimed to understand the effect of α-TOH and mechanism involved in inducing the ALI. Lipopolysaccharide (LPS) is injected into the trachea of mice to generate ALI mouse models. α-TOH was used to administrate the mice intragastrically to detect the expression of inflammatory factors and antioxidant molecules by enzyme linked immunosorbent assay, hematoxylin-eosin staining and immunohistochemical staining. Mouse alveolar epithelial cell line (MLE-12 cells) was used to determine the effect of α-TOH on alveolar epithelial cells. Inflammatory factors such as, interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α shows significant increase in the lung tissues of the mice induced by LPS and reduction in the expressions of superoxide dismutase (SOD)1/2 and glutathione peroxidase (GSH-Px). After treatment with α-TOH, the inflammation and oxidative stress levels shows substantial reduction in the lung tissues of the mice. Moreover, α-TOH also increases the proliferation ability of MLE-12 cells in vitro and reduces apoptosis level. In addition, α-TOH reduces p65 phosphorylation and nuclear translocation in alveolar epithelial cells in vivo and in vitro, thus, inhibiting the activity of the nuclear factor kappa-B (NF-κB) signaling pathway. α-TOH reduces the inflammation and oxidative stress of lung tissue by inhibiting the NF-κB signaling pathway, thereby alleviating the LPS-induced ALI.

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Vitamin E Decreases Cytotoxicity and Mitigates Inflammatory and Oxidative Stress Responses in a Ferret Organotypic Brain Slice Model of Neonatal Hypoxia-Ischemia

Sarah Kolnik, Kylie Corry, Kate Hildahl, Jeremy Filteau, Olivia White, Olivia Brandon, Lily Farid, AnnaMarie Shearlock, Daniel Moralejo, Sandra E Juul, Elizabeth Nance, Thomas R Wood

Dev Neurosci . 2022 Feb 8. doi: 10.1159/000522485. Online ahead of print.

Abstract

The gyrencephalic ferret brain is an excellent model in which to study hypoxia-ischemia (HI), a significant contributor to neurological injury in neonates. Vitamin E, an essential fat-soluble antioxidant, reduces oxidative stress and inflammation in both animal models and neonates. The aim of this study was to assess the effects of Vitamin E after oxygen glucose deprivation (OGD) in an organotypic ferret brain slice model of neonatal HI. We hypothesized that Vitamin E would decrease cytotoxicity, inflammation, and oxidative stress in OGD-exposed brain slices. Term-equivalent ferrets were sacrificed at postnatal (P) day 21-23 and 300µM whole hemisphere brain slices were obtained. During a 24h rest period, slices were cultured in either non-treated control conditions or with Erastin, a promotor of oxidative stress. Slices were then exposed to 2h of OGD followed by Vitamin E (25-100 IU/kg), Erastin (10µM) or Ferrostatin (1µM), an inhibitor of ferroptosis. Relative cytotoxicity was determined using an LDH assay, cell death was quantified via nuclear propidium iodide (PI) staining, oxidative stress was quantified via cellular GSH (glutathione) levels and target genes responsive to oxidative stress and inflammation were evaluated by qRT-PCR. OGD increased cytotoxicity, which was significantly reduced by treatment with Vitamin E. Vitamin E also preserved GSH after OGD and decreased amplification of certain markers of oxidative stress (CHAC1, SLC7A11) and inflammation (TNF-alpha, IL-8). Vitamin E remained protective after pretreatment with Erastin and was more protective than Ferrostatin, presumably due to its added anti-inflammatory properties. Results from the ferret whole hemisphere OGD model support the premise that Vitamin E neuroprotection is mediated by restoring GSH and acutely decreasing inflammation and oxidative stress after neonatal HI brain injury.

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Gamma-tocopherol, a major form of vitamin E in diets: Insights into antioxidant and anti-inflammatory effects, mechanisms, and roles in disease management

Qing Jiang, Suji Im, James G Wagner, Michelle L Hernandez, David B Peden

Free Radic Biol Med . 2022 Jan;178:347-359. doi: 10.1016/j.freeradbiomed.2021.12.012. Epub 2021 Dec 9.

Abstract

γ-Tocopherol (γT) is a major form of vitamin E in the US diet and the second most abundant vitamin E in the blood and tissues, while α-tocopherol (αT) is the predominant vitamin E in tissues. During the last >25 years, research has revealed that γT has unique antioxidant and anti-inflammatory activities relevant to disease prevention compared to αT. While both compounds are potent lipophilic antioxidants, γT but not αT can trap reactive nitrogen species by forming 5-nitro-γT, and appears to show superior protection of mitochondrial function. γT inhibits ionophore-stimulated leukotrienes by blocking 5-lipoxygenase (5-LOX) translocation in leukocytes, decreases cyclooxygenase-2 (COX-2)-catalyzed prostaglandins in macrophages and blocks the growth of cancer cells but not healthy cells. For these activities, γT is stronger than αT. Moreover, γT is more extensively metabolized than αT via cytochrome P-450 (CYP4F2)-initiated side-chain oxidation, which leads to formation of metabolites including 13′-carboxychromanol (13′-COOH) and carboxyethyl-hydroxychroman (γ-CEHC). 13′-COOH and γ-CEHC are shown to be the predominant metabolites found in feces and urine, respectively. Interestingly, γ-CEHC has natriuretic activity and 13′-COOH inhibits both COX-1/-2 and 5-LOX activity. Consistent with these mechanistic findings of γT and metabolites, studies show that supplementation of γT mitigates inflammation and disease symptoms in animal models with induced inflammation, asthma and cancer. In addition, supplementation of γT decreased inflammation markers in patients with kidney diseases and mild asthma. These observations support that γT may be useful against inflammation-associated diseases.

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