Vitamin E is an antioxidant that can help fight free radicals, which are molecules that damage the DNA in cells. People can usually get adequate vitamin E from their diet, but it is also available in the form of supplements and skin care products.
Blog Archives
Vitamin E and Lactobacillus Provide Protective Effects Against Liver Injury Induced by HgCl 2: Role of CHOP, GPR87, and mTOR Proteins
Ahlam Alhusaini, Shahad Alghilani, Waad Alhuqbani, Iman H Hasan
Dose Response . 2021 Apr 26;19(2):15593258211011360. doi: 10.1177/15593258211011360. eCollection Apr-Jun 2021.
Abstract
Background and objective: Mercury is one of the most harmful heavy metals and its toxicity causes severe multi-organ dysfunction. This study was designed to explore novel molecular pathways involved in the hepatoprotective effect of vitamin E (Vit-E) and Lactobacillius plantarum (Lac-B) against mercury toxicity.
Method: Acute hepatotoxicity was induced by administration of high dose of mercuric chloride (HgCl2) in male rats, Vit-E or/and Lac-B were given along with HgCl2 for 2 weeks. The effects of those antioxidants were studied focusing on their anti-apoptotic, anti-oxidative stress and anti-inflammatory eficacies. Histopathological examinations were also conducted.
Results: The administration of HgCl2 induced liver injury which manifested by elevation in serum ALT and AST. Liver MDA, caspase-3 and TNF-α levels were markedly increased; whereas, GSH level and SOD activity were declined. HgCl2 significantly elevated the expressions of hepatic CHOP, GPR87, NF-κB and mTOR. Histopathological examination revealed massive hepatocyte degeneration following HgCl2 administration. Treatment with Vit-E or/and Lac-B restored the normal levels of the previously mentioned parameters, as well as improved hepatic architecture.
Conclusion: Vit-E and Lac-B provided protective effect against HgCl2-induced hepatotoxicity via reduction of oxidative stress and inflammation, and downregulation of CHOP, GPR87, NF-κB and mTOR proteins’ expressions.
Vitamin E: necessary nutrient for neural development and cognitive function
Maret G Traber
Proc Nutr Soc . 2021 Apr 26;1-8. doi: 10.1017/S0029665121000914. Online ahead of print.
Abstract
Vitamin E, discovered in 1922, is essential for pregnant rats to carry their babies to term. However, 100 years later, the molecular mechanisms for the vitamin E requirement during embryogenesis remain unknown. Vitamin E’s role during pregnancy has been difficult to study and thus, a vitamin E-deficient (E-) zebrafish embryo model was developed. Vitamin E deficiency in zebrafish embryos initiates lipid peroxidation, depletes a specific phospholipid (DHA-phosphatidyl choline), causes secondary deficiencies of choline, betaine and critical thiols (such as glutathione), and dysregulates energy metabolism. Vitamin E deficiency not only distorts the carefully programmed development of the nervous system, but it leads to defects in several developing organs. Both the α-tocopherol transfer protein and vitamin E are necessary for embryonic development, neurogenesis and cognition in this model and likely in human embryos. Elucidation of the control mechanisms for the cellular and metabolic pathways involved in the molecular dysregulation caused by vitamin E deficiency will lead to important insights into abnormal neurogenesis and embryonic malformations.
Effects of delta-tocotrienol supplementation on Glycemic Control, oxidative stress, inflammatory biomarkers and miRNA expression in type 2 diabetes mellitus: A randomized control trial
Wajiha Mahjabeen, Dilshad Ahmed Khan, Shakeel Ahmed Mirza, Muhammad Amjad Pervez
Phytother Res . 2021 Apr 25. doi: 10.1002/ptr.7113. Online ahead of print.
Abstract
The study aimed to ascertain the effects of delta-tocotrienol (δT3) supplementation on glycemic control, oxidative stress, inflammation and related micro-ribonucleic acid (miRNA) expression in patients with type 2 diabetes mellitus (T2DM). Total 110 patients of T2DM on oral hypoglycemic agents, were randomly divided into tocotrienol and placebo groups and given 250 mg δT3 or cellulose soft gel capsule once daily respectively for 24 weeks. Glycemic control, oxidative stress, inflammatory biomarkers, and miRNAs expression were measured in serum at baseline and end of the intervention by using standard laboratory methods. Compared to the placebo, δT3 supplementation resulted in a significant (p ≤ .05) reduction [mean difference (95% confidence interval)] in plasma glucose [-0.48 (-0.65, -0.30)], insulin [-1.19 (-1.51, -0.87)], homeostatic model assessment of insulin resistance [-0.67 (-0.86, -0.49)], glycosylated hemoglobin [-0.53 (-0.79, -0.28)], malondialdehyde [-0.34 (-0.45, -0.22)], high sensitive-C-reactive protein[-0.35 (-0.54, -0.16)], tumor necrosis factor-alpha [-1.22 (-1.62, -0.83)], and interleukin-6[-2.30 (-2.91, -1.68)]. More than twofold downregulation in miRNA-375, miRNA-34a, miRNA-21, and upregulation in miRNA-126, miRNA-132 expression was observed in the δT3 group compared to the placebo. The study demonstrated that δT3 supplementation in addition to oral hypoglycemic agents, improved glycemic control, inflammation, oxidative stress, and miRNA expression in T2DM without any adverse effect. Thus, δT3 might be considered as an effective dietary supplement to prevent long-term diabetic complications.
Inhibition of endoplasmic reticulum stress and activation of autophagy-protect intestinal and renal tissues from western diet-induced dysbiosis and abrogate inflammatory response to LPS: role of vitamin E
A M Shamseldeen, M Hamzawy, N A Mahmoud, L Rashed, S S Kamar, L A Harb, N Sharawy
J Biol Regul Homeost Agents . Mar-Apr 2021;35(2):457-471. doi: 10.23812/20-693-A.
Abstract
Diet pattern is an emerging risk factor for renal disease. The mechanism by which high-fat high fructose (western) diet mediates renal injury is not yet fully understood. The objective of the present study was to investigate the relationship between endoplasmic reticulum (ER) stress and autophagy in the development of renal impairment and aggravation of the inflammatory response. Eighty male rats were randomly divided into four groups as follows: a standard diet-fed (ConD), a high-fat high fructose diet fed (HFHF-V), ConD fed and orally supplemented with vitamin E (ConD-E), and HFHF fed and orally supplemented vitamin E (HFHF-E). After 12 weeks, either lipopolysaccharide (LPS) or saline was injected. We found that upregulation of endoplasmic reticulum stress-related proteins rendered the cells susceptible to injury induced by dysbiosis and microbiota-derived metabolites. A downregulation of autophagy and upregulation of caspase-12 resulted in the loss of intestinal integrity and renal tubular injury. Maintained ER stress also increased the inflammatory response to LPS. In contrast, vitamin E effectively ameliorated ER stress and promoted autophagy to protect intestinal and renal tissues. Our results provide insight into the influences of sustained ER stress activation and autophagy inhibition on the development of renal injury, which may contribute also to the enhanced inflammatory response.
Vitamin E beyond Its Antioxidant Label
Anca Ungurianu, Anca Zanfirescu, Georgiana Nițulescu, Denisa Margină
Antioxidants (Basel) . 2021 Apr 21;10(5):634. doi: 10.3390/antiox10050634.
Abstract
Vitamin E, comprising tocopherols and tocotrienols, is mainly known as an antioxidant. The aim of this review is to summarize the molecular mechanisms and signaling pathways linked to inflammation and malignancy modulated by its vitamers. Preclinical reports highlighted a myriad of cellular effects like modulating the synthesis of pro-inflammatory molecules and oxidative stress response, inhibiting the NF-κB pathway, regulating cell cycle, and apoptosis. Furthermore, animal-based models have shown that these molecules affect the activity of various enzymes and signaling pathways, such as MAPK, PI3K/Akt/mTOR, JAK/STAT, and NF-κB, acting as the underlying mechanisms of their reported anti-inflammatory, neuroprotective, and anti-cancer effects. In clinical settings, not all of these were proven, with reports varying considerably. Nonetheless, vitamin E was shown to improve redox and inflammatory status in healthy, diabetic, and metabolic syndrome subjects. The anti-cancer effects were inconsistent, with both pro- and anti-malignant being reported. Regarding its neuroprotective properties, several studies have shown protective effects suggesting vitamin E as a potential prevention and therapeutic (as adjuvant) tool. However, source and dosage greatly influence the observed effects, with bioavailability seemingly a key factor in obtaining the preferred outcome. We conclude that this group of molecules presents exciting potential for the prevention and treatment of diseases with an inflammatory, redox, or malignant component.
Effect of prolonged whole-body hyperthermia on adult male rat testes and the protective role of vitamin C and E: A histological and biochemical study
Suhaila A Qari, Ahlam A Alahmadi, Soad S Ali, Zuhair M Mohammedsaleh, Rabee F A Ibrahim, Nagla A El-Shitany
Andrologia . 2021 Apr 20;e14075. doi: 10.1111/and.14075. Online ahead of print.
Abstract
Hyperthermia (HT) is a significant risk factor for male infertility. Most researchers investigated the effect of localized and short-term HT on male fertility. This study aimed to assess the harmful impacts of prolonged and generalized HT on testicular histology and ultrastructure in rats. The possible protective effects of vitamin E (Vit E), Vit C, and their combination were also investigated. Thirty male adult Wister rats were used (5 groups). 1- control, 2- HT, 3- Vit C, 4- Vit E, and 5- Vit C + Vit E. Rats in groups 2-5 were subjected to HT (41°C), 1 hr daily for 2 weeks. HT-induced a significant decrease in body weight gain, food and water intake, and serum testosterone. HT showed a damaging effect on the testicular and coda epididymis tissue. HT significantly (p ≤ .05) produced oxidative stress (decreased serum catalase (145.49 ± 8.98), glutathione peroxidase (20.27 ± 4.46), superoxide dismutase (2.68 ± 0.54), and reduced glutathione (5.18 ± 0.33), and increased malondialdehyde (9.46 ± 1.55). Vit E alone and combined with Vit C, significantly protected the gonads against the deleterious effects of HT. The results recommended that prolonged HT of the whole body is harmful to male fertility. Prophylactic therapy with Vit E could help decrease the HT-induced male gonadal harm.
Inhibition of 20-hydroxyeicosatetraenoic acid biosynthesis by vitamin E analogs in human and bovine cytochrome P450 microsomes
Matthew J Kuhn, Lorraine M Sordillo
J Anim Physiol Anim Nutr (Berl) . 2021 Apr 14. doi: 10.1111/jpn.13547. Online ahead of print.
Abstract
Dairy cattle are predisposed to disease around the time of calving due to dysfunctional inflammatory responses. Oxylipids are lipid-derived mediators that regulate all aspects of the inflammatory response, and shifts in oxylipid profiles are correlated with disease risk. For example, 20-hydroxyeicosatetraenoic acid (HETE) is an oxylipid derived from cytochrome P450 enzymes (CYP450) found at significantly greater concentrations around calving and during clinical disease. Biosynthesis of 20-HETE occurs almost exclusively from two specific CYP450 of which CYP450 family four sub-family F member two (CYP4F2) is the major contributor to 20-HETE production in humans. To further study the activities of 20-HETE and potentially reduce its production in vivo, mitigation methods must be explored. Additional substrates of CYP4F2, such as vitamin E, are known to both increase and decrease the metabolism of other CYP4F2 substrates. This study aimed to determine whether vitamin E analogs may reduce the production of 20-HETE through competition for CYP4F2 activity in human CYP4F2, bovine-kidney and bovine-mammary microsomes. Gamma-tocopherol reduced 20-HETE production from human and bovine-kidney microsomes (35.3% and 27.5%, respectively) whereas γ-tocotrienol only reduced 20-HETE production from human microsomes (40.1%). Finally, bovine-mammary microsomes did not produce a quantifiable amount of 20-HETE, suggesting basal mammary CYP4F2 activity may not be a significant contributor to 20-HETE found in milk. Together, these data show that analogs of vitamin E can reduce the production of 20-HETE, potentially through competition with arachidonic acid for metabolism by CYP4F2, posing a potential means for limiting 20-HETE production during clinical diseases of dairy cattle.
The Combination of Berberine, Tocotrienols and Coffee Extracts Improves Metabolic Profile and Liver Steatosis by the Modulation of Gut Microbiota and Hepatic miR-122 and miR-34a Expression in Mice
Valentina Cossiga, Vincenzo Lembo, Cecilia Nigro, Paola Mirra, Claudia Miele, Valeria D'Argenio, Alessia Leone, Giovanna Mazzone, Iolanda Veneruso, Maria Guido, Francesco Beguinot, Nicola Caporaso, Filomena Morisco
Nutrients . 2021 Apr 13;13(4):1281. doi: 10.3390/nu13041281.
Abstract
Non-alcoholic-fatty liver disease (NAFLD) is spreading worldwide. Specific drugs for NAFLD are not yet available, even if some plant extracts show beneficial properties. We evaluated the effects of a combination, composed by Berberis Aristata, Elaeis Guineensis and Coffea Canephora, on the development of obesity, hepatic steatosis, insulin-resistance and on the modulation of hepatic microRNAs (miRNA) levels and microbiota composition in a mouse model of liver damage. C57BL/6 mice were fed with standard diet (SD, n = 8), high fat diet (HFD, n = 8) or HFD plus plant extracts (HFD+E, n = 8) for 24 weeks. Liver expression of miR-122 and miR-34a was evaluated by quantitativePCR. Microbiome analysis was performed on cecal content by 16S rRNA sequencing. HFD+E-mice showed lower body weight (p < 0.01), amelioration of insulin-sensitivity (p = 0.021), total cholesterol (p = 0.014), low-density-lipoprotein-cholesterol (p < 0.001), alanine-aminotransferase (p = 0.038) and hepatic steatosis compared to HFD-mice. While a decrease of hepatic miR-122 and increase of miR-34a were observed in HFD-mice compared to SD-mice, both these miRNAs had similar levels to SD-mice in HFD+E-mice. Moreover, a different microbial composition was found between SD- and HFD-mice, with a partial rescue of dysbiosis in HFD+E-mice. This combination of plant extracts had a beneficial effect on HFD-induced NAFLD by the modulation of miR-122, miR-34a and gut microbiome.
Dietary Annatto-Extracted Tocotrienol Reduces Inflammation and Oxidative Stress, and Improves Macronutrient Metabolism in Obese Mice: A Metabolic Profiling Study
Chwan-Li Shen, Sivapriya Ramamoorthy, Gurvinder Kaur, Jannette M Dufour, Rui Wang, Huanbiao Mo, Bruce A Watkins
Nutrients . 2021 Apr 13;13(4):1267. doi: 10.3390/nu13041267.
Abstract
Obesity and its related complications are a world-wide health problem. Dietary tocotrienols (TT) have been shown to improve obesity-associated metabolic disorders, such as hypercholesterolemia, hyperglycemia, and gut dysbiosis. This study examined the hypothesis that the antioxidant capacity of TT alters metabolites of oxidative stress and improves systemic metabolism. C57BL/6J mice were fed either a high-fat diet (HFD control) or HFD supplemented with 800 mg annatto-extracted TT/kg (HFD+TT800) for 14 weeks. Sera from obese mice were examined by non-targeted metabolite analysis using UHPLC/MS. Compared to the HFD group, the HFD+TT800 group had higher levels of serum metabolites, essential amino acids (lysine and methionine), sphingomyelins, phosphatidylcholine, lysophospholipids, and vitamins (pantothenate, pyridoxamine, pyridoxal, and retinol). TT-treated mice had lowered levels of serum metabolites, dicarboxylic fatty acids, and inflammatory/oxidative stress markers (trimethylamine N-oxide, kynurenate, 12,13-DiHOME, and 13-HODE + 9-HODE) compared to the control. The results suggest that TT supplementation lowered inflammation and oxidative stress (oxidized glutathione and GSH/GSSH) and improved macronutrient metabolism (carbohydrates) in obese mice. Thus, TT actions on metabolites were beneficial in reducing obesity-associated hypercholesterolemia/hyperglycemia. The effects of a non-toxic dose of TT in mice support the potential for clinical applications in obesity and metabolic disease.