Effect Of Alpha-tocopherol Supplementation Research Articles

Effects of Alpha-Tocopherol Supplementation on Adult Mices: Biochemichal Status, Histopathological Analysis and Review of Genes Modulated by Vitamin E

Vitamin E (VE) is an antioxydant defense system and a signaling molecule which has been the subject of various clinical trials in cancer chemoprevention or in adjuvant therapy after chemotherapy. In some circunstances it is indexed to act as a pro-oxidant inducing adverse effects such as progesssion of cancer metastasis or diabetes. The objective of this work is firstly to investigated the effect of VE (α-T) supplementation on mices, in way to evaluate the risk in developping diabetes and secondly to make review on vitamin E modulated genes. The study was performed on 32 adult albino mices in which alpha-tocopherol was administred at different doses. After, blood biochemical paramaters status has been analysed. Renal damages were researched by histopathological analysis. We have made review on VE modulated genes through indexed articles in genetic databases, PubMed Central and Google scholar. An inadequate status of blood biochemical paramaters especially, glucose level, hyperlipidemia and a hypercreatininemia has been observed. Renal damages with modifications in structures were noted. A list of genes modulated by VE, which could explain mechanisms by which α-T- induced diabetes could appear was highlighted. The study shows that high doses of α-T supplement resulted in disorder of biochemical parameters, with dysfunction of renal tissue and development of diabetes.

Effect of Alpha-Tocopherol Supplementation in TCM199 Medium on In Vitro Maturation and Cleavage of Buffalo Oocytes

An experiment was conducted to assess the effect of supplementing α-tocopherol at two different concentrations to the in vitro maturation (IVM) medium (TCM 199 culture medium) on in vitro maturation and cleavage of buffalo oocytes. Ovaries were collected from local slaughter house. Oocytes were collected by aspiration method and were matured in IVM medium (T0, control), IVM medium supplemented with α-tocopherol @ 10 μg/ml (T1) and IVM medium supplemented with α-tocopherol @ 20 μg/ml (T2). The mean cytoplasmic maturation rate was 82.39 ± 0.81, 88.81 ± 1.08, 81.67 ± 1.82 % and nuclear maturation rate was 62.50 ± 8.33, 87.50 ± 5.59, 66.66 ± 7.68 % in T0, T1 and T2 groups, respectively. The fertilized oocytes reaching 2-cell and 4-cell stages of cleavage for T0, T1 and T2 groups were 14.92 ± 1.52, 32.39 ± 1.01 and 16.39 ± 1.25 %, respectively. Significantly (p less than 0.05) higher level of cytoplasmic maturation rate, nuclear maturation rate and cleavage rate was observed in IVM medium supplemented with α-tocopherol @10 μg/ml than other two groups.

Impact of castration with or without alpha-tocopherol supplementation on the urethral sphincter of rats

To analyze the impact of low levels of testosterone induced by orchiectomy and the effect of alpha-tocopherol supplementation on oxidative stress in the urethral sphincter. Forty male Wistar rats weighing 250-300 g were divided into four groups with 10 each: Sham group; Orchiectomy group: bilateral orchiectomy; Orchiectomy-pre-Tocopherol group: bilateral orchiectomy preceded by alpha-tocopherol supplementation for four weeks; Orchiectomy-full-Tocopherol group: bilateral orchiectomy with alpha-tocopherol supplementation for four weeks preceding the procedure and for eight weeks afterwards. At the protocol end, animals were euthanized and had the sphincter analyzed stereologically focusing on collagen and muscle fibers percentage. Oxidative stress levels were determined using 8-epi-PGF2. The 8-epi-PGF2 levels were statistically higher (p < 0.0003) in the Orchiectomy group compared to others groups while Sham and Orchiectomy-full-Tocopherol groups presented statistically similar values (p = 0.52). Collagen volumetric densities were significantly lower in Sham and Orchiectomy-full-Tocopherol groups (p < 0.022). Sham group presented statistically greater muscle fiber percent. Castration caused oxidative stress in the urethral sphincter complex, with increased collagen deposition. Alpha-tocopherol had a protective effect and its supplementation for twelve weeks provided the greatest protection.

The effects of alpha-tocopherol supplementation on fracture healing in a postmenopausal osteoporotic rat model

OBJECTIVE:Osteoporosis increases the risk of bone fractures and may impair fracture healing. The aim of this study was to investigate whether alpha-tocopherol can improve the late-phase fracture healing of osteoporotic bones in ovariectomized rats.METHOD:In total, 24 female Sprague-Dawley rats were divided into three groups. The first group was sham-operated, and the other two groups were ovariectomized. After two months, the right femora of the rats were fractured under anesthesia and internally repaired with K-wires. The sham-operated and ovariectomized control rat groups were administered olive oil (a vehicle), whereas 60 mg/kg of alpha-tocopherol was administered via oral gavage to the alpha-tocopherol group for six days per week over the course of 8 weeks. The rats were sacrificed, and the femora were dissected out. Computed tomography scans and X-rays were performed to assess fracture healing and callus staging, followed by the assessment of callus strengths through the biomechanical testing of the bones.RESULTS:Significantly higher callus volume and callus staging were observed in the ovariectomized control group compared with the sham-operated and alpha-tocopherol groups. The ovariectomized control group also had significantly lower fracture healing scores than the sham-operated group. There were no differences between the alpha-tocopherol and sham-operated groups with respect to the above parameters. The healed femora of the ovariectomized control group demonstrated significantly lower load and strain parameters than the healed femora of the sham-operated group. Alpha-tocopherol supplementation was not able to restore these biomechanical properties.CONCLUSION:Alpha-tocopherol supplementation appeared to promote bone fracture healing in osteoporotic rats but failed to restore the strength of the fractured bone.

Vitamin E Forms in Alzheimer's Disease: A Review of Controversial and Clinical Experiences

Vitamin E is a collective term for eight naturally occurring compounds, four tocopherols (alpha-, beta-, gamma-, and delta-) and four tocotrienols (alpha-, beta-, gamma-, and delta-). Although it is the major form of vitamin E in US diets, gamma-tocopherol receives little attention when compared to alpha-tocopherol, which is generally found in supplements and most studied for its effects on progression of cognitive impairment. Many clinical trials had been conducted with vitamin E and neurodegenerative disorders, with controversial results, including a recent study which disproves the benefit of vitamin E for Mild Cognitive Impairment and Alzheimer's Disease. This study examined the alpha-tocopherol supplement instead of gamma–tocopherol. Gamma-tocopherol has been found to be more effective in scavenging free radicals and nitrogen oxygen species that cause inflammation; both of these are components of neurodegenerative disorders. Secondly, the use of alpha-tocopherol supplements significantly reduces serum gamma-tocopherol, and this may have important biological effects. Therefore, any potential health benefits of alpha–tocopherol supplements may be offset by deleterious changes in the bioavailability of other forms of tocopherols and tocotrienols. This might account for the null effects of alpha tocopherol supplementation in Mild Cognitive Impairment and Alzheimer's Disease.

Effects of α-Tocopherol on Oxidative Status and Metabolic Profile in Overweight Women

Despite extensive research, the effects of alpha-tocopherol supplementation remain controversial. Few studies have been focused on obese and overweight people. We examined the effects of alpha-tocopherol (AT) on the oxidative status and metabolic profile in overweight women. Sixteen overweight women between the ages of 40-60 years old, received AT, 800 IU/day during 12 weeks, followed by a 6-week washout period. Blood samples were taken at the beginning and then every 6 weeks until the end of the study. AT, retinol, malondialdehyde (MDA), total antioxidant status (TAS), selenium-dependent glutathione peroxidase (GPx) and CuZn-superoxide dismutase (SOD) were quantified to evaluate the oxidative stress. The metabolic profile was estimated by measuring glycated hemoglobin (HbA1c) in erythrocytes and glucose, phosphate, magnesium, lipid and lipoprotein concentrations in serum. Under AT administration HbA1c, serum- MDA levels and erythrocyte GPx activity were markedly reduced. TAS, AT and Mg2+ concentrations in serum and SOD activity in erythrocytes were higher after AT treatment. Body weight; glucose, lipid and retinol concentrations, or blood cells count were unchanged. Lipid peroxidation was considerably reduced in AT treated women and also improved serum antioxidant status was observed, but the imbalanced response between erythrocyte SOD and GPx activities could affect normal response to oxidative stress.

Effect of alpha-tocopherol supplementation on plasma homocysteine and oxidative stress in highly trained athletes before and after exhaustive exercise

The interrelationship between physical exercise, antioxidant supplementation, oxidative stress and plasma levels of homocysteine (Hcy) has not been adequately examined. The purpose of this study was to examine the effect of 2 months of vitamin E supplementation (800 IU/day alpha-tocopherol) (E) or placebo (P) in 38 triathletes on plasma Hcy concentrations, antioxidant potential and oxidative stress. It was hypothesized that vitamin E supplementation would reduce plasma Hcy and oxidative stress markers compared to placebo. Blood samples were collected 1 day prior to the race, immediately postrace and 1.5 h postrace. Plasma alpha-tocopherol was 75% higher ( P<.001) in E versus P prerace (24.1±1.1 and 13.8±1.1 μmol/L, respectively), and this group difference was maintained throughout the race. Cortisol was significantly increased in both E and P ( P<.001), but there was no difference in the pattern of change. There were no significant time, group or interaction effects on plasma Hcy concentrations between E and P. Plasma F 2-isoprostanes increased 181% versus 97% during the race in E versus P, and lipid hydroperoxides were significantly elevated ( P=.009) 1.5 h postrace in E versus P. Plasma antioxidant potential was significantly higher 1.5 h postrace in E versus P ( P=.039). This study indicates that prolonged large doses of alpha-tocopherol supplementation did not affect plasma Hcy concentrations and exhibited pro-oxidant characteristics in highly trained athletes during exhaustive exercise.

In Vivo Rates of Skeletal Muscle Protein Synthesis in Rats Are Decreased by Acute Ethanol Treatment but Are Not Ameliorated by Supplemental α-Tocopherol

Some studies have shown that reductions in tissue protein synthesis, under a variety of cytotoxic conditions, are ameliorated by alpha-tocopherol (ATC) supplementation. We have also shown evidence of increased oxidative stress and reduced protein synthesis rates in alcohol-exposed muscle. Serum levels of ATC fall and rates of muscle protein synthesis are reduced in patients with alcoholic myopathy. We therefore tested the hypothesis that treatment with ATC could ameliorate the ethanol-induced changes in muscle protein synthesis, a contributory event in the pathogenesis of alcoholic muscle disease. Studies were carried out on gastrocnemius (Type II fiber-predominant and usually considered representative of the musculature as a whole), soleus (Type I fiber-predominant) and plantaris (Type II fiber-predominant) muscles. For comparative purposes, we also investigated the liver. Young male Wistar rats (90 g body weight) were injected intraperitoneally (i.p.) daily with ATC (30 mg/kg body weight) in Intralipid fat emulsion (0.1 mL/100 g body, i.p.) for 5 d. Controls were similarly injected with the Intralipid vehicle alone. After ATC supplementation, rats were given ethanol (75 mmol/kg body weight, i.p., 2.5 h) or saline (0.15 mol/L NaCl, i. p.). Fractional rates of tissue protein synthesis (i.e., the percentage of the tissue protein pool renewed each day, k(s), %/d) and RNA activities [i.e., the amount of protein synthesis each day per unit RNA, k(RNA), mg protein/d/mg RNA)] were then measured. Supplementation increased ATC concentrations in plasma, gastrocnemius and liver. There was no effect of ATC supplementation alone on k(s) in any of the tissues. ATC supplementation in the absence of alcohol increased k(RNA) in the plantaris muscle. In nonsupplemented groups, acute ethanol treatment reduced skeletal muscle (soleus, plantaris and gastrocnemius) k(s). Hepatic k(s) was not altered by ethanol, although ATC concentrations in this tissue increased due to ethanol. However, none of the changes in muscle k(s) or k(RNA) due to ethanol were significantly affected by ATC supplementation. In conclusion, ATC supplementation does not appear beneficial in ameliorating acute alcohol toxicity in skeletal muscle as defined by reductions in protein synthesis.

Effect of alpha-tocopherol supplementation on the impactof aflatoxin B 1 on the testes of rats

Rats were given aflatoxin B1 (7.5 microg/200 g b.w.) and alpha-tocopherol (0.9 mg/200 g b.w.) for 14 days oral intubation to investigate the effect of alpha-tocopherol on the toxicity of aflatoxin B1 on rat's testes. There were significant alterations in testicular sorbitol dehydrogenase, lactic dehydrogenase, glucose-6-phosphate dehydrogenase, gamma glutamyl transpeptidase; reduced quality of sperm and marked pathological changes in the testis of rats given aflatoxin B1 alone. Alpha-tocopherol supplementation increased the aflatoxin blood level. A reduction in the toxicity of free radicals by alpha-tocopherol in association with a reduction in aflatoxin metabolism seem to be responsible for the protective influence observed.

The effects of alpha tocopherol supplementation on monocyte function. Decreased lipid oxidation, interleukin 1 beta secretion, and monocyte adhesion to endothelium.

Low levels of alpha tocopherol are related to a higher incidence of cardiovascular disease and increased intake appears to afford protection against cardiovascular disease. In addition to decreasing LDL oxidation, alpha tocopherol may exert intracellular effects on cells crucial in atherogenesis, such as monocytes. Hence, the aim of this study was to test the effect of alpha tocopherol supplementation on monocyte function relevant to atherogenesis. Monocyte function was assessed in 21 healthy subjects at baseline, after 8 wk of supplementation with d-alpha tocopherol (1,200 IU/d) and after a 6-wk washout phase. The release of reactive oxygen species (superoxide anion, hydrogen peroxide), lipid oxidation, release of the potentially atherogenic cytokine, interleukin 1 beta, and monocyte-endothelial adhesion were studied in the resting state and after activation of the monocytes with lipopolysaccharide at 0, 8, and 14 wk. There was a 2.5-fold increase in plasma lipid-standardized and monocyte alpha tocopherol levels in the supplemented phase. After alpha tocopherol supplementation, there were significant decreases in release of reactive oxygen species, lipid oxidation, IL-1 beta secretion, and monocyte-endothelial cell adhesion, both in resting and activated cells compared with baseline and washout phases. Studies with the protein kinase C inhibitor, Calphostin C, suggest that the inhibition of reactive oxygen species release and lipid oxidation is due to an inhibition of protein kinase C activity by alpha tocopherol. Thus, this study provides novel evidence for an intracellular effect of alpha tocopherol in monocytes that is antiatherogenic.

Phospholipid fatty acids of brain and liver are modified by alpha-tocopherol and dietary fat in growing chicks.

Dietary fatty acids modify phospholipid fatty acids in brain and liver of growing chickens post-hatching. The effect of vitamin E deficiency on this process is unknown and may be relevant to the pathogenesis of chick nutritional encephalomalacia (NE). Therefore laying hens received a diet low in vitamin E (10 mg alpha-tocopherol/kg feed). Resulting chicks were assigned to nine dietary groups each fed with either oleic (18:1n-9, 58 g/kg), linoleic (18:2n-6, 57 g/kg) or linolenic (18:3n-3, 56 g/kg) acid together with 5. 25 or 125 mg alpha-tocopherol/kg feed. NE affecting the cerebellum only occurred in the group given linoleic acid and 5 mg alpha-tocopherol/kg. In 1-d-old chicks and after 1 and 2 weeks the phospholipid fatty acid composition of liver, cerebrum and cerebellum (additionally after 3 weeks) was determined. The feed fatty acids were incorporated into the liver very efficiently during the first week of life. Unsaturation of liver membranes decreased in the order dietary linolenic > linoleic > oleic acid. In liver, also, the effect of alpha-tocopherol supplementation on phospholipid fatty acids was most pronounced. The unsaturation index increased during deficiency, whereas n-9 fatty acids decreased. In the chicken brain the alterations were delayed and less distinct. The cerebellum phospholipids were rich in n-9 fatty acids and as a whole more saturated in comparison with the cerebrum. Cerebellar unsaturation increased when linolenic or linoleic acid was given. However, NE-producing dietary conditions were not accompanied by specific alterations in cerebellar phospholipid fatty acids due to the alpha-tocopherol content of the diet. Rather the alterations of membrane fatty acids in the liver seem to play a role in the pathogenesis of NE.

Mammary dysplasia: Endocrine parameters and tocopherol therapy

The effect of alpha tocopherol supplementation on serum hormones was studies in women with clinically confirmed mammary dysplasia and age-matched controls. Serum samples collected at monthly intervals on the 21st day of the menstrual cycle for a period of four months were analyzed for estradiol, progesterone, testosterone and dehydroepiandrosterone by radioimmunoassay. Eighty-five percent of the patients showed objective and subjective remission from the disease. Alpha tocopherol supplementation reduced the serum dehydroepiandrosterone levels of patients without affecting the concentrations of other hormones.