Α-tocopherol Supplementation Research Articles

Ameliorative effect of α-tocopherol and curcumin against the deleterious effects of hydrogenated (thermally oxidized) rice bran oil in rats

Rice bran oil (RBO) is known for its health benefits due to its high content of natural antioxidants like tocotrienols, tocopherols, and oryzanols, which combat oxidative stress and inflammation. However, repeated heating of RBO above 110°C leads to degradation, forming harmful oxidative components and reducing its antioxidant content. This study aimed to investigate the effects of long-term consumption of thermally oxidized RBO on rats and the potential protective effects of curcumin and α-tocopherol supplementation. RBO was subjected to oxidative degradation through repeated frying cycles at temperatures ranging from 100°C to 180°C for 45 days. Physicochemical and phytochemical parameters of the oxidized RBO were analyzed. In vivo experiments evaluated serum biochemical, hematological, and histopathological parameters, along with oxidative and inflammatory responses in rats fed with oxidized RBO for 45 days. Results showed that thermal oxidation at 180°C significantly altered the chemical composition of RBO, increasing oxidative markers and reducing nutritional components. Consumption of oxidized RBO led to decreased body weight gain, elevated levels of various biochemical markers indicating liver and kidney dysfunction, hyperlipidemia, and increased oxidative and inflammatory damage in rats. However, supplementation with curcumin and α-tocopherol effectively mitigated these harmful effects. In conclusion, long-term consumption of thermally oxidized RBO negatively affects health parameters in rats, but fortification with curcumin and α-tocopherol helps alleviate these adverse effects

Vitamin E alleviates chlorpyrifos induced glutathione depletion, lipid peroxidation and iron accumulation to inhibit ferroptosis in hepatocytes and mitigate toxicity in zebrafish

Organophosphates, a widely used group of pesticides, can cause severe toxicity in human beings and other non-target organisms. Liver, being the primary site for xenobiotic metabolism, is extremely vulnerable to xenobiotic-induced toxicity. Considering the numerous vital functions performed by the liver, including xenobiotic detoxification, protecting this organ from the ubiquitous pesticides in our food and environment is essential for maintaining homeostasis.In this study, we have investigated the impact of the organophosphate pesticide, Chlorpyrifos (CPF), on zebrafish liver at a concentration (300 μg/L) which is environmentally realistic. We have also demonstrated the role of dietary supplementation of α-tocopherol or Vitamin E (Vit E) (500 mg/kg feed) in mitigating pesticide-induced liver toxicity. Mechanistically, we showed that Vit E resulted in significant elevation of the Nrf2 and its downstream antioxidant enzyme activities and gene expressions, especially that of GST and GPx, resulting in reduction of CPF-induced intracellular lipid ROS and hepatic LPO. Further interrogation, such as analysis of GSH: GSSG ratio, intracellular iron concentration, iron metabolizing genes, mitochondrial dysfunction etc. revealed that CPF induces ferroptosis which can be reversed by Vit E supplementation. Ultimately, reduced concentration of CPF in zebrafish serum and flesh highlighted the role of Vit E in ameliorating CPF toxicity.

α-Tocopherol inhibits atherogenesis and improves cardiac function in mice independently of its antioxidant properties.

The impact of α-tocopherol on atherosclerosis is unclear and controversial. While some studies suggest potential benefits, such as antioxidant properties that may reduce oxidative stress, other studies indicate no significant preventive effects. The intricate interplay of various factors, including dosage, individual differences, and study methodologies, contributes to the ongoing uncertainty surrounding α-tocopherol's role in atherosclerosis. Further research is needed to clarify its impact and establish clearer guidelines. Therefore, we aimed to evaluate the impact of α-tocopherol on atherogenesis in ApoE-/- fibrillin (Fbn)1C1039G/+ mice, which is a unique mouse model of advanced atherosclerosis with typical features, such as large necrotic cores, high levels of inflammation, and intraplaque neovascularization, that resemble the unstable phenotype of human plaques. ApoE-/- Fbn1C1039G+/- mice were fed a western-type diet (WD) supplemented with a high dose of α-tocopherol (500 mg/kg diet), while control mice were fed a WD containing a low dose of α-tocopherol (50 mg/kg diet). The high dose of α-tocopherol reduced plaque thickness and necrotic core area in the right common carotid artery (RCCA) after 24 weeks WD. Moreover, α-tocopherol decreased plaque formation and intraplaque neovascularization in the RCCA. In addition to its antiatherogenic effect, chronic supplementation of α-tocopherol improved cardiac function in ApoE-/- Fbn1C1039G/+ mice. However, chronic supplementation of α-tocopherol did not decrease lipid peroxidation. On the contrary, α-tocopherol acted as a prooxidant by increasing plasma levels of oxidized LDL and plaque malondialdehyde, an end product of lipid peroxidation. Our data indicate that α-tocopherol inhibits atherogenesis and improves cardiac function independent of its antioxidant properties.

Effects of α-Tocopherol on chilled quality parameters of Tharparkar bull semen extended in Lecithin and Tris based egg yolk extender

In this experiment, four healthy Tharparkar Cattle Bulls, 4-5 years aged were used. Total 52 (n=13) ejaculates were collected, and the semen samples having motility, morphology and viability ≥70% were processed and extended into BIOXcell­­­TM and Tris Based Egg Yolk extender supplemented with and without α-tocopherol (Vitamin E) 0.02 Mm/ml. Pre-thawed assessment of motility, morphology, viability and membrane integrity with BIOXcell­­­TM + α-tocopherol (Vitamin E) (79.09±0.87, 86.13±0.79, 82.13±1.20, 81.40±0.77) showed improved quality parameters as compared to Tris+ α-tocopherol (Vitamin E) (74.69±0.94, 82.81±1.00, 77.63±1.26, 77.31±1.01), BIOXcellTM (73.55±1.20, 80.81±0.96, 76.02±1.28, 75.31±1.20) and Tris (71.72±1.28, 78.90±1.01, 74.04±1.31, 73.18±1.29) respectively. In conclusion supplementation of α-tocopherol (Vitamin E) improves the Pre thawed quality parameters i.e. Motility, Morphology, Viability and Membrane Integrity of Tharparkar Bull semen extended in BIOXcell­­­TM and Tris Based Egg Yolk extender.

Synergistic impact of α-linolenic acid and α-tocopherol on in vitro maturation and culture of buffalo oocytes.

The objective of the current study was to investigate the synergistic impact of α-Tocopherol and α-Linolenic acid (100 µM) on IVM and IVC of Nili Ravi buffalo oocytes. Oocytes were obtained from the ovaries of slaughtered buffaloes within two hours after slaughter and brought to laboratory. Buffalo cumulus oocyte complexes were placed randomly in the five experimental groups included; GROUP 1: Maturation media (MM) + 100 µM ALA (control), GROUP 2: MM + 100 µM ALA + 50μM α-Tocopherol, GROUP 3: MM + 100 µM ALA + 100μM α-Tocopherol, GROUP 4: MM + 100 µM ALA + 200 μM α-Tocopherol and GROUP 5: MM + 100 µM ALA + 300 μM α-Tocopherol under an atmosphere of 5% CO2 in air at 38.5 °C for 22-24 h. Cumulus expansion and nuclear maturation status was determined (Experiment 1). In experiment 2, oocytes were matured as in experiment 1. The matured oocytes were then fertilized in Tyrode's Albumin Lactate Pyruvate (TALP) medium for about 20 h and cultured in synthetic oviductal fluid (SOF) medium to determine effect of α-Linolenic acid (100 µM) and α-Tocopherol in IVM medium on IVC of presumptive zygotes. To study the effect of α-Linolenic acid (100 µM) in IVM media and increasing concentration of α-tocopherol in the culture media on early embryo development (Experiment 3), the presumptive zygotes were randomly distributed into the five experimental groups with increasing concentration of α-tocopherol in culture media. Higher percentage of MII stage oocytes in experiment 1(65.2±2.0), embryos at morula stage in experiment 2 (30.4±1.5) and experiment 3 (22.2±2.0) were obtained. However, overall results for cumulus cell expansion, maturation of oocyte to MII stage and subsequent embryo development among treatments remain statistically similar (P > 0.05). Supplementation of α-tocopherol in maturation media having α-Linolenic acid and/or in embryo culture media did not further enhance in vitro maturation of oocyte or embryo production.

Stress-Protective Role of Dietary α-Tocopherol Supplementation in Longfin Yellowtail (Seriola rivoliana) Juveniles

Aquaculture practices expose fish to several factors that may generate stress, modifying the balance between the production of reactive oxygen species (ROS) and the activity of antioxidant defenses that induce cell damage. Alpha-tocopherol (VE) improves the antioxidant capacity against ROS production in fish. A 50-day trial with longfin yellowtail (Seriola rivoliana) juveniles was conducted to compare the dietary supplementation of 500 mg/kg of VE against a control diet without VE supplementation on growth, lymphoid tissue enzymatic activity, immune-system-related gene expression, and the histology of the liver and spleen. Growth, weight gain, specific growth rate, feed conversion rate, and survival did not show significant differences (p > 0.05) among treatments. Fish fed with an α-tocopherol-enriched diet showed a higher enzymatic activity of superoxide dismutase in the liver (p < 0.05) and a lower percentage of melanomacrophage coverage area in the lymphoid organs (p < 0.05). Overexpression was observed of MyD88 and il-10 in the spleen, and il-1b in the liver in fish fed 500 mg/kg of VE, as well as overexpression of Toll-like 3 in the head kidney, spleen, and liver in fish fed the control diet. Dietary supplementation with VE reduces the effects of oxidative stress and improves lymphoid tissue defense and immune-related gene expression in S. rivoliana.

Vitamin E - a scoping review for Nordic Nutrition Recommendations 2023.

Current evidence suggests that dietary vitamin E (as α-tocopherol) intake has a beneficial role in preventing certain chronic diseases. In contrast, there is no clear evidence for the benefit of α-tocopherol supplements in a generally healthy population. Deficiency symptoms are rare and mainly occur due to genetic or other factors affecting α-tocopherol absorption and/or metabolism, rather than a low α-tocopherol intake. No qualified systematic review was identified by the NNR2023 project for updating the dietary reference values (DRV).

α-Tocopherol reduces VLDL secretion through modulation of intracellular ER-to-Golgi transport of VLDL.

Avoiding hepatic steatosis is crucial for preventing liver dysfunction, and one mechanism by which this is accomplished is through synchronization of the rate of very low density lipoprotein (VLDL) synthesis with its secretion. Endoplasmic reticulum (ER)-to-Golgi transport of nascent VLDL is the rate-limiting step in its secretion and is mediated by the VLDL transport vesicle (VTV). Recent in vivo studies have indicated that α-tocopherol (α-T) supplementation can reverse steatosis in nonalcoholic fatty liver disease, but its effects on hepatic lipoprotein metabolism are poorly understood. Here, we investigated the impact of α-T on hepatic VLDL synthesis, secretion, and intracellular ER-to-Golgi VLDL trafficking using an in vitro model. Pulse-chase assays using [3H]-oleic acid and 100 µmol/L α-T demonstrated a disruption of early VLDL synthesis, resulting in enhanced apolipoprotein B-100 expression, decreased expression in markers for VTV budding, ER-to-Golgi VLDL transport, and reduced VLDL secretion. Additionally, an in vitro VTV budding assay indicated a significant decrease in VTV production and VTV-Golgi fusion. Confocal imaging of lipid droplet (LD) localization revealed a decrease in overall LD retention, diminished presence of ER-associated LDs, and an increase in Golgi-level LD retention. We conclude that α-T disrupts ER-to-Golgi VLDL transport by modulating the expression of specific proteins and thus reduces VLDL secretion.

Vitamin E and cardiovascular diseases: an interest to public health?

Cardiovascular diseases (CVD) are the leading cause of death worldwide. From this perspective, the role of vitamin E and its metabolites in preventing CVD has been studied, being supported by the findings that low vitamin E concentrations are associated with an increased risk of cardiovascular events. Despite this, no studies have analysed the co-existence of vitamin E deficiency (VED) and CVD on the basis of population studies. Facing that, this study summarises information on the relationship between vitamin E status and CVD, providing a basis for understanding the determining and protective factors for its development. VED may be a public health problem since it has been observed to vary from 0·6% to 55·5% worldwide, with higher percentages in Asia and Europe, where CVD mortality rates stand out. Intervention studies with α-tocopherol supplementation do not confirm cardioprotective action of vitamin E, which may reflect that α-tocopherol alone does not provide cardiovascular protection to individuals, but the consumption of all isomers found in food. Considering that low concentrations of α-tocopherol can lead to a higher susceptibility to diseases involving oxidative stress in the population, in addition to the high and growing prevalence of CVD and VED, it is essential to investigate or reinterpret the mechanisms of action of vitamin E and its metabolites in the cardiovascular process to better understand the co-existence of CVD and VED. It is also important to implement public health policies and programmes aimed at promoting the consumption of natural food sources of vitamin E and healthy fats.

Lung microbial dysbiosis during early life promotes predisposition to allergic asthma.

Abstract Background: Allergic asthma is associated with lung microbial dysbiosis. We hypothesized that the microbiome from the lungs of allergy-predisposed mouse pups is sufficient to predispose pups to development of allergy. Allergic inflammation in pups of allergic dams is blocked by α-tocopherol supplementation of the dam during gestation and nursing, but it is unknown whether α-tocopherol alters microbial composition of the lung. Methodology: Mouse pups were predisposed to allergy by inducing allergy in the mothers. Microbiome was separated from the bronchoalveolar lavage (BAL) of pups of allergic and non-allergic mothers and transferred intranasally at postnatal day 4. 16S rRNA sequencing was performed on the Illumina MiSeq platform. Results: Compared to pups born to non-allergic dams and dams administered with a-tocopherol supplementation, mouse pups born to allergic dams had elevated abundance of several genera of the γ-Proteobacteria, Firmicutes, and Verrucomicrobia (p<0.05). There was decreased abundance of genera from Bacteroides, Firmicutes, and α-Proteobacteria (p<0.05). Transfer of lung microbiome from neonates of allergic dams to neonates of non-allergic dams was sufficient to confer responsiveness to allergen in the recipient pups. Neonates of allergic dams were not protected from development of allergy by transfer of donor lung microbiome from neonates of non-allergic dams or neonates of αT-supplemented allergic dams. The donor microbiome from pups of allergic mothers colonized the pup lung, suggesting that early life detrimental bacterial species persists. Conclusion: The lung microbiome from allergy-predisposed pups is dominant and sufficient for enhanced neonate responsiveness to allergen. Supported by grants from NIH (R01AI127695)

Effect of α-tocopherol in the vitrification medium on the viability, lipid peroxidation, expression of key developmental, apoptotic and stress-related genes in ovine secondary follicles.

The present study aimed to evaluate the effect of α-tocopherol on viability, lipid peroxidation and the expression of apoptosis, stress and development-related genes in the vitrified sheep secondary follicles. Ovarian secondary follicles (200-300 μm) were isolated and distributed separately to the vitrification treatment and supplemented with 5 mM, 10 mM, 20 mM and 30 mM of α-tocopherol (while the control fresh group was without vitrification and supplementation of α-tocopherol). After a week, the follicles were thawed and evaluated for follicular viability by trypan blue dye exclusion method, lipid peroxidation and gene expression studies. The results showed that the vitrification with 10 and 20 mM of α-tocopherol positively affected (p < .05) the viability of vitrified follicles in comparison with vitrified ones without α-tocopherol but the higher concentration of α-tocopherol, i.e., 30 mM negatively affected the viability (p < .05) in comparison with the 10 and 20 mM of α-tocopherol groups. The malondialdehyde (MDA) levels were significantly (p < .05) higher in the vitrified without α-tocopherol group in comparison to the vitrified with 20 mM of α-tocopherol group. The expression of apoptotic-related gene, BCL2L1 was significantly higher in 10 mM α-tocopherol group compared to the control fresh and CASPASE 3, 9 expressions were significantly higher in the vitrified group when compared to the vitrified with 10 mM α-tocopherol group. Expressions of BAX, BAD, BAK, BMP-15 and GDF-9 showed no significant difference among the groups. The mRNA expression of SOD1 was significantly higher in the vitrified without α-tocopherol group when compared to other groups. We conclude that the supplementation of 10 and 20 mM α-tocopherol in vitrification solution was the efficient vitrification procedure for the vitrification of ovine secondary follicles.

Effect of α-Tocopherol on Viability, Lipid Peroxidation and Oxidative Stress of Cryopreserved Ovine Preantral Follicle

Vitrification of preantral follicles is a promising technique to preserve female fertility. The aim of the present study was to evaluate the effect of supplementation of α-tocopherol in the vitrification solution on the viability, lipid peroxidation and mRNA expression of superoxide dismutases (SOD1 and SOD2) in vitrified cultured ovine preantral follicles at day-6 and day-12. Preantral follicles (200-300 µm) were isolated from the ovine ovaries by the mechanical method and were distributed separately to the vitrification medium supplemented with 10 mM and 20 mM of α-tocopherol. After a week, the follicles were thawed and analyzed for follicular viability by trypan blue dye exclusion method and subjected to in vitro culture (IVC) for 6 and 12 days. Our results revealed that the significant increase (p&lt;0.05) of viability in 20 mM α-tocopherolsupplemented vitrified group when compared to the vitrified without α-tocopherol group. On day-6 of IVC, malondialdehyde (MDA) concentration was significantly(p&lt;0.05) higher in vitrified group without α-tocopherol in comparison to vitrified supplemented with 20 mM of α-tocopherol and control fresh groups. However, no significant difference in MDA content was found among the groups at day-12. The mRNA expression level of SOD1 at day-6 was significantly (p&lt;0.05) higher in vitrified with 20 mM of α-tocopherol and control fresh groups compared to the vitrified without α-tocopherol and with10 mM α-tocopherol groups. The expression pattern of SOD2 was significantly (p&lt;0.05) higher in control fresh group compared to the other groups at day-6 and day-12 of IVC.We conclude that lowering the vitrification-induced lipid peroxidation of preantral follicles by α-tocopherol at 20 mM concentration may be mediated by increasing SOD expression during IVC.

Acacia mearnsii tannin extract and α-tocopherol supplementation in lamb diet: Effects on growth performance, serum lipid peroxidation and meat quality

This study investigated the effects of supplementing lamb diets with plant bioactive compounds α-tocopherol, tannin and the association of both on lamb growth, blood and meat characteristics. Forty male lambs were housed in individual pens and assigned to four treatment groups (10 animals/group), where, for 62 d, they were fed: 1) a basal diet with soybean hulls, soybean meal and corn (Control); 2) the Control diet containing α-tocopherol (Tocopherol); 3) the Control diet containing Acacia mearnsii tannin extract (Tannin); and 4) The Control diet containing A. mearnsii extract and α-tocopherol (Tannin + tocopherol). The Tannin and Tannin + tocopherol treatments resulted in lower cold carcass weight. The concentration of α-tocopherol in the muscle was higher in Tocopherol and Tannin + tocopherol treatments. Meat lipid oxidation, after 7 days of storage, was lower (P ≤ 0.05) in lambs fed Tocopherol and Tannin + tocopherol than in the Tannin treatment, while the treatments with Tannin experienced a trend of reduced serum lipid peroxidation. Tannin diets modified the meat fatty acid profile, with an increase in C17:0 and in the PUFA/MUFA ratio and a decrease in the enzymatic Δ9-desaturase activity (C16 and C18) and in the MUFA/SFA ratio, in addition to promoting a increasing in the sum of PUFAs. Lamb supplementation with α-tocopherol and A. mearnsii tannin are alternatives capable of improving meat quality and reducing serum lipid peroxidation.

Cholesterol accumulation in hepatocytes mediates IRE1/p38 branch of endoplasmic reticulum stress to promote nonalcoholic steatohepatitis.

Non-alcoholic fatty liver disease (NAFLD), based on the elevating obesity incidence, is one of the major health issue worldwide. Transition from NAFLD to non-alcoholic steatohepatitis (NASH) is driven by increased apoptosis and is relevant to higher morbidity rates. In regard to limited understanding on cholesterol mediated hepatocyte alterations in NALFD/NASH transition, we investigated endoplasmic reticulum (ER) stress and related apoptosis. Our findings suggest that cholesterol upregulates ER stress and enhances C/EBP homologous protein (CHOP) either in hypercholesterolemic rabbits or in hepatocytes treated with liposome-cholesterol complex. Mechanistically, cholesterol accumulation in hepatocytes activates IRE1/p38 branch of ER stress, stimulating CHOP levels. In liver tissues of cholesterol fed rabbits, α-tocopherol supplementation decreased IRE1/p38/CHOP activation and prevented NASH development. Thus, our study provides a critical role of hepatocyte cholesterol in inducing IRE1/p38/CHOP pathway and suggests novel candidates for therapeutic targets against NASH.

α-tocopherol supplementation of allergic mothers blocks neonate lung microbiome dysbiosis during initiation of neonate allergy

α-tocopherol supplementation of allergic mothers blocks neonate lung microbiome dysbiosis during initiation of neonate allergy

Effect of retinol and α-tocopherol supplementation on photoreceptor and retinal ganglion cell apoptosis in diabetic rats model

BackgroundDiabetic retinopathy (DR) is the most common microvascular complication of diabetes. Retinol and α-tocopherol of diabetic models prevent the damage of photoreceptor and retinal ganglion cells (RGC) caused by hyperglycemia.ObjectiveThis study aims to examine the effect of retinol and α-tocopherol on photoreceptor and RGC densities and the expression of caspase-3 and -7 on the retinal layers of the diabetic rat model.MethodsAlloxan 150 mg/kg body weight single dose was used to develop animal models, which were separated into eight groups. These consist of one group without intervention (group 1), one positive control with only induced alloxan (group 2), and others receiving retinol (group 3 and 6), α-tocopherol (group 4 and 7), or their combination (group 5 and 8). Furthermore, histopathological examination was performed using Hematoxylin–Eosin staining to evaluate the photoreceptor and RGC densities, while immunohistochemistry staining evaluated the caspase-3 and -7 expressions.ResultsIn the treatment group, the highest and lowest densities were identified in diabetic rats given α-tocopherol (group 7) and retinol (group 3) respectively. The caspase-3 and -7 expression showed that the group given α-tocopherol (group 7) had the lowest value.ConclusionIn diabetic rats, retinol and α-tocopherol compounds maintained densities and prevented photoreceptor and RGC death. However, α-tocopherol was more promising than retinol or combinations in the prevention of retinal cells apoptosis.

The Influence of Rumen-Protected Choline and α-tocopherol Supplementation on Early Lactating Dairy Cows Metabolism.

It is well documented that choline is known as one of the essential ingredients of phospholipids. Choline acts as a determinative element for appropriate cell membrane functions. On the other hand α-tocopherol (Vit E) is a fat-soluble vitamin. This vitamin acts as a strong antioxidant in the living body's defense system against oxidative stress. Lipid peroxidation in peripartum and early lactating cows is significantly increased while the level of serum Vit E is decreases dramatically. These concomitant physiological changes demonstrate a higher level of oxidative stress subsequently leads to serious health issues in dairy cows. Therefore, the present research was designed to investigate the following items in dairy cattle: 1) evaluation of the possible changes in serum protein fractions, and 2) comparing the oxidative status of orally RPC and vitamin E supplementation in dairy cows in early lactation period. In the current study 30 early lactating primiparous and multiparous Holstein cows (body condition score (BCS)=2.51 ± 0.10) were used beginning five weeks postpartum. All the animals were randomly divided in to three groups (n=10) (number of lactation=2.61). The animals were randomly assigned to receive one of the following treatments. Group 1 served as control group were not received any supplement. The second group was supplemented with 90 g/d of RPC (Reashre Choline, Balchem, USA). The third group was administrated 4400 IU/d vitamin E (Roche, Vitamins Ltd; Switzerland). In the current study, serum protein electrophoresis showed four main fractions as follows: albumin, α-globulin, β-globulin, and γ-globulin. The recorded data showed that the percentages of albumin and γ-globulin fractions were higher in treated groups compared to the control group. In the animals supplementing with RPC and vitamin E the percentages of serum albumin increased to the value of 37. 70±1.63 and 38.21±1.28 respectively compare to the control group (34.69±1.21), which were significant (P<0.05).

Detection of diabetic cardiomyopathy in Egyptian children and adolescents with longstanding Type 1 diabetes and evaluating the effect of α-tocopherol supplementation on cardiac functions after 1 year; a single center prospective study.

IntroductionDiabetic cardiomyopathy (DCM) is a serious complication that frequently occurs in patients with type 1 diabetes (T1D) necessitating early diagnosis. The aim of the current study was to detect subclinical DCM in Egyptian children and adolescents with T1D and evaluate the effect of antioxidants on myocardial dysfunction.Material and methodsThe current prospective observational cohort study included 81 T1D patients (9-20 years old) with diabetes duration &gt; 4 years compared to 50 age and sex matched non-diabetic controls. Serum N-terminal prohormone of brain natriuretic peptide (NT-proBNP) was assessed in addition to conventional echocardiography, tissue Doppler imaging (TDI) and speckle tracking echocardiography (STE). Patients with myocardial dysfunction were supplemented with vitamin E (α-tocopherol) as an antioxidant for 1 year, then follow up echocardiography was done.ResultsNT-proBNP was elevated in 73 (90.1%) patients, 50.6% had left ventricular (LV) diastolic dysfunction, 14.8% had right ventricular (RV) diastolic dysfunction, 84% had LV systolic dysfunction and 91.4% had RV systolic dysfunction with statistically significant difference compared to controls. There was a significant negative correlation between LV global longitudinal strain (GLS) and NT-proBNP (p&lt;0.001, r=-0.796). ROC curve analysis showed that NT-proBNP at a cut-off point ≥ 195 ng/ml detected LV systolic dysfunction function with 89.7% sensitivity and 84.6% specificity. Follow up after one year of α-tocopherol supplementation revealed significant improvement in LV systolic and diastolic functions as well as RV systolic dysfunction.ConclusionsNT-proBNP and non-conventional echocardiography were useful in early detection of subclinical cardiomyopathy in patients with T1D. Antioxidant treatment improved subclinical myocardial dysfunction in T1D patients.

Response to different sources of vitamin E orally injected and to various doses of vitamin E in calf starter on the plasma vitamin E level in calves around weaning

Calves often face a lower plasma vitamin E level than the recommended level (3 µg/ml for adult cows) after weaning, a level which has been related to a good immune response. Two experiments were performed to determine the most effective source and level of vitamin E to be included in a calf starter to maintain the plasma vitamin E level above the recommended level after weaning. Experiment 1 (Exp 1) and experiment 2 (Exp 2) included a total of 32 and 40 calves, respectively, from 2 weeks before weaning until 2 weeks after weaning. In Exp 1, calves were orally injected a daily dose of different vitamin E sources including, no α-tocopherol (0 dose; Control), 200 mg/d of RRR-α-tocopherol (ALC), 200 mg/d of RRR-α-tocopheryl acetate (ACT), or 200 mg/d of all-rac-α-tocopheryl acetate (SYN). In Exp 2, a dose response study was carried out with 0, 60, 120, and 200 mg/kg of ALC in a pelleted calf starter. Final BW (100 ± 16 and 86 ± 11 kg) and average daily gain (956 ± 303 and 839 ± 176 g/d in Exp 1 and 2, respectively; mean ± SD) were unaffected by either source or level of α-tocopherol. In Exp 1, the plasma RRR-α-tocopherol level was affected by α-tocopherol source (P < 0.001), week (P < 0.001), and interaction between them (P < 0.001). At weaning time, the plasma RRR-α-tocopherol was 2.7, 2.1, 1.1, and 0.8 μg/ml in ALC, ACT, SYN, and Control, respectively. In Exp 2, the plasma α-tocopherol level was affected by ALC dose (P = 0.04), week (P < 0.001), and a tendency for an interaction between them was observed (P = 0.06). At weaning, a 36, 31, and 28% reduction in plasma α-tocopherol level was observed compared to the beginning of the experiment with 0, 60, and 120 mg/kg of ALC, respectively; however, with 200 mg/kg of ALC, a 9% increase in the plasma α-tocopherol level was observed. In addition, 200 mg/kg of ALC was able to maintain plasma α-tocopherol after weaning higher than the recommended level. The results showed that the ALC was the most efficient source of α-tocopherol supplementation to be used in a calf starter. In addition, the 200 mg/kg of ALC in the calf starter was the only effective dose to maintain the postweaning plasma vitamin E concentration at the recommended level after weaning and α-tocopherol similar to that observed before weaning.

A 28-year prospective analysis of serum vitamin E, vitamin E-related genetic variation and risk of prostate cancer.

Objective:Investigate the relationship between serum α-tocopherol concentration and long-term risk of prostate cancer, and evaluate the interaction with vitamin E–related genetic variants and their polygenic risk score (PRS).Methods:We conducted a biochemical analysis of 29 102 male Finnish smokers in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study. Serum α-tocopherol was measured at baseline using high-performance liquid chromatography, and 2 724 prostate cancer cases were identified during 28 years of follow-up. Cox proportional hazards models examined whether serum α-tocopherol concentrations were associated with prostate cancer risk. Among 8 383 participants, three SNPs related to vitamin E status (rs964184, rs2108622, and rs11057830) were examined to determine whether they modified the relationship between serum α-tocopherol concentrations and prostate cancer risk, both individually and as a PRS using logistic regression models.Results:No association was observed between serum α-tocopherol and prostate cancer risk (fifth quintile (Q5) versus Q1 hazard ratio (HR)=0.87, 95% confidence interval (95% CI) 0.75, 1.02; p-trend=0.57). Though no interactions were seen by population characteristics, high α-tocopherol concentration was associated with reduced prostate cancer risk among the trial α-tocopherol supplementation group (Q5 quintile versus Q1 HR=0.79, 95% CI 0.64, 0.99). Finally, no associated interaction between the three SNPs or their PRS and prostate cancer risk was observed.Conclusion:Although there was a weak inverse association between α-tocopherol concentration and prostate cancer risk over nearly three decades, our findings suggest that men receiving the trial α-tocopherol supplementation who had higher baseline serum α-tocopherol concentration experienced reduced prostate cancer risk. Vitamin E–related genotypes did not modify the serum α-tocopherol-prostate cancer risk association.