Effects of excess vitamin E on rat teeth

Summary The purpose of this investigation was to determine if the feeding of excess vitamin E during tooth formation changes the mineral content of teeth. Purified diets containing 0, 250, and 2500 IU vitamin E per kg were fed to 15-day pregnant rats and continued during lactation and to the pups after weaning. Rats were killed at 2 and 4 weeks after weaning. Incisors and molars were weighed, ashed, and the percent of calcium, magnesium, and phosphorus was determined. Feeding of excess vitamin E (2500 IU/kg diet) had no deleterious effect on percent ash or mineral composition of rat teeth. In fact, molars from rats fed excess vitamin E had slightly higher calcium and phosphorus levels. Such differences were also apparent but to a lesser extent in the dentin and enamel composition.     

Effects of vitamin E and vitamin C on male infertility: a meta-analysis

International Urology and Nephrology - The efficacy of the antioxidants vitamin E (VitE) and vitamin C (VitC) on male infertility is uncertain. Therefore, this research systematically assessed the...     

The effect of vitamin E & vitamin B on sperm function in rat varicocele model

We assessed the effect of vitamin E and vitamin B (Vit E & Vit B) and their combination on sperm functional parameters in the rat varicocele model. Male rats (n = 120) were divided into control (n = 30), sham (n = 30) and varicocele induction (n = 60) groups. After 2 months, 10 rats from each group were sacrificed to verify varicocele model. This part of results showed that sperm parameters, DNA damage, lipid peroxidation and residual histone were adversely effected in the varicocele group. From the 50 remaining rats in varicocele group, 10 rats received Vit B complex (6, 9.6, 30.4, 9.6 and 0.006 mg/kg for B6, B2, B9, B1 and B12 respectively), 10 rats received Vit E (40 mg/kg), 10 rats received Vit B & E, 10 rats only received water and 10 rats were only received sesame oil as a solvent for Vit E, for 2 months. From 40 remaining rats in control and sham groups, 20 rats only received water and other 20 rats only received sesame oil for 2 months. Then, all the aforementioned parameters were assessed. These results showed that Vit B antioxidant was more efficient in improvement of sperm parameters, chromatin integrity and lipid peroxidation in varicocelized rats compared with Vit E.     

回补维生素E对维生素E缺乏不孕大鼠妊娠结局的影响

目的研究在植入过程回补维生素E对维生素E缺乏不孕(VED)大鼠妊娠结局的影响。方法从出生后11d开始喂养维生素E缺乏的食物,喂养6个月后建立VED大鼠模型。在模型大鼠交配后5.5d、6.5d、7.5d分别灌胃500mg/kg的维生素E回补,以非VED大鼠为对照组,在回补0h、4h、8h、12h、16h、20h和24h观察维生素E的浓度变化,并于交配后19.5d统计大鼠子宫的着床点个数、活胎个数和胎鼠体重变化。结果 VED大鼠在回补4h后血浆中维生素E的浓度为13.54±3.81μg/ml,达到正常水平;分别在交配后5.5d、6.5d、7.5d回补维生素E的VED大鼠妊娠率分别为80%、60%、40%(对照组均为100%),着床点个数分别为9.3±1.1、8.5±0.5和8.4±1.4(对照组为12.7±0.5、13.0±2.2和12.7±1.2),活胎个数分别为5.0±2.0、4.0±2.3和2.0±2.4(对照组为12.3±0.5、12.7±2.4和11.3±1.7),均显著低于对照组(P0.05);交配后5.5d回补组胎鼠体重与对照组相比无统计学差异(P0.05),交配后6.5d和7.5d回补组胎鼠体重显著低于对照组(分别为1.74±0.55g和1.63±0.68g vs.2.16±0.18g和2.19±0.21g)(P0.01)。结论在植入过程回补维生素E可部分挽救由于维生素E缺乏所导致的不孕;随着回补时间的延后,回补维生素E对妊娠结局挽救的效果明显下降。     

维生素E拮抗铬致大鼠睾丸毒性作用的实验研究

为研究维生素Ｅ对铬酸钾（Ｋ２ＣｒＯ４）所致大鼠睾丸毒性的影响，将大鼠分为４组，其中３组口服Ｋ２ＣｒＯ４（１０ｍｇ／ｋｇ体重），第二组加服维生素Ｅ（５ｍｇ／ｋｇ），第三组按２０ｍｇ／ｋｇ体重加服维生素Ｅ，连续服药３０天后，通过光镜检查，结果发现：单纯服用Ｋ２ＣｒＯ４１０ｍｇ／ｋｇ组的大鼠睾丸曲精管不同程度变性，管内生精细胞数目减少、缺如，精子形成少或者无。而用Ｋ２ＣｒＯ４（１０ｍｇ／ｋｇ）染毒同时加     

Effects of intraperitoneally administered vitamin E and selenium on calcium oxalate renal stone formation: experimental study in rat

Forty-eight Wistar rats were treated for 3 weeks with water containing 0.7% ethylene-glycol and divided into four groups. The first group, used as control, has received sodium chloride at 1 ml/100 g BW daily. The second group was intraperitoneally injected with selenium at 10 micrograms/d per 100 g BW as NaSeO3 for 3 weeks. The third group was intraperitoneally administered with 15 mg Vit E/d per 100 g BW as alpha-tocopherol acetate for 3 weeks. The last group was simultaneously administered vitamin E and Se at the same doses and periods as the precedent groups. One day before the end of the treatment, each animal was placed in a metabolic cage for collection of 24 h urine samples and determination of urinary creatinin, urea, calcium, magnesium, phosphate and oxalate levels. Immediately thereafter, all the rats were anesthetized and aortic blood was collected to determine the same parameters as in urine. The kidneys were also removed to determine calcium oxalate deposits, dry weight and to conduct a histological examination. Our results showed decreased ionic product and increased magnesium fractional reabsorption in the group receiving only selenium and in the group receiving selenium in combination with vitamin E, in comparison with the control animals. In view of the knowledge concerning the same protective action of Vit E and selenium, regardless of tubular membrane alteration, the absence of any inhibitory effect of Vit E on calcium oxalate formation suggests that selenium, like other minerals, could be stuck onto the crystal surface and would inhibit induction of new crystals, growth and aggregation.     

Effects of vitamin E on bone turnover markers among US postmenopausal women

Increased oxidative stress and inflammation resulting from aging and declining estrogen levels can lead to increased bone loss in postmenopausal women. Alpha‐tocopherol and gamma‐tocopherol, the two predominant isomers of vitamin E, have antioxidant and anti‐inflammatory properties, but their effects on bone metabolism have not been well studied in humans. We examined the associations between dietary and total (diet and supplements) alpha‐tocopherol intake, serum alpha‐tocopherol and gamma‐tocopherol levels and their ratio, and bone turnover markers (BTMs) among postmenopausal women aged ≥45 years. We used cross‐sectional data from the National Health and Nutrition Examination Survey 1999–2002. Multiple regression models with adjustments for relevant confounders were used to examine the associations between intake and serum levels of tocopherols, and serum bone‐specific alkaline phosphatase (BAP), a biomarker of bone formation, and urinary N‐telopeptides/creatinine (uNTx/Cr), a biomarker of bone resorption. The study sample included 497 postmenopausal women who were not taking estrogen, steroids, or osteoporosis medications, were free from kidney and liver disease, cancer, and rheumatoid arthritis, and were fasting >9 hours prior to examination. Participants had a mean age of 65.5 ± 0.6 years and over 45% used vitamin E (alpha‐tocopherol) supplements in the past month. Vitamin E supplement users had significantly lower serum gamma‐tocopherol, higher serum alpha‐tocopherol levels, and higher ratio of serum alpha‐tocopherol to gamma‐tocopherol than nonusers. High serum gamma‐tocopherol levels and low ratio of serum alpha‐tocopherol to gamma‐tocopherol were associated with increased BAP levels (p < 0.01 for both). There were no associations between any of the vitamin E variables and uNTx/Cr. In conclusion, we hypothesize that gamma‐tocopherol may uncouple bone turnover, resulting in more bone formation than resorption. Vitamin E supplements in the form of alpha‐tocopherol suppress serum gamma‐tocopherol levels and may have negative effects on bone formation. Further research is needed to investigate the potential anabolic effect of gamma‐tocopherol from food sources on bone. © 2012 American Society for Bone and Mineral Research.     

Effects of large dose vitamin E supplementation on anemia in hemodialysis patients

In order to clarify the effect of vitamin E (alpha-tocopherol) on anemia and the osmotic fragility of red blood cells (RBC) plasma and RBC levels of vitamin E were measured in 30 regular dialysis patients before and after oral supplementation of vitamin E, 600 mg daily for 30 days. Plasma levels of vitamin E were in the normal range (10.67 +/- 0.85, 9.73 +/- 0.77 microgram/ml) but RBC levels in packed red cells were significantly lower than healthy controls (0.57 +/- 0.05, 0.45 +/- 0.07 microgram/ml). Oral supplementation of vitamin E increased both plasma (20.37 +/- 1.61 micrograms/ml) and RBC vitamin E (1.56 +/- 0.11 micrograms/ml) in packed red cells, while in unsupplemented patients, vitamin E levels remained unchanged. In patients receiving vitamin E, mean osmolarities at the beginning and end of hemolysis decreased from 102.8 +/- 0.9 to 98.9 +/- 0.7 and 72.1 +/- 1.1 to 67.4 +/- 0.8 mosm/l, respectively. In addition, the hematocrit increased from 26.1 +/- 1.0 to 28.1 +/- 1.2%. These changes are statistically significant (less than 0.05). In conclusion, the oral supplementation of vitamin E could be of clinical benefit in correcting anemia in regular dialysis patients by reducing the fragility of RBCs.     

Effects of testosterone and vitamin E on the antioxidant system in rabbit testis

The aim of the study was to investigate the effects of testosterone propionate and vitamin E on the antioxidant system in the testis. Thirty-two male New Zealand White rabbits were randomly divided into four groups. The first group was used as control. The second group was injected with testosterone propionate, the third group vitamin E and the fourth group vitamin E and testosterone propionate combination. All treatments were carried out during 6 weeks and oxidative parameters were evaluated in homogenized testicular tissue. The levels of vitamin E and the activity of glutathione peroxidase were lower (P < 0.05) in the testosterone group than in controls. However, vitamin C and malondialdehyde levels were higher (P < 0.05) in this group than in controls. The levels of reduced glutathione, beta-carotene, vitamin C and E increased, but malondialdehyde levels decreased in the vitamin E group, when compared with controls (P < 0.05). Vitamin E and beta-carotene levels were significantly higher (P < 0.05) in the combination group than in testosterone group. However, MDA levels were lower (P < 0.05) in combination group than in the testosterone group. In conclusion, administration of testosterone propionate led to a significant elevation of oxidative stress. Vitamin E is quite an effective antioxidant which protects rabbit testis against lipid peroxidation, and, testosterone-induced lipid peroxidation could be improved by additional vitamin E treatment.     

Growth inhibition of rat mesangial cells by high glucose: effect of vitamin E

Background. We aimed to examine both whether vitamin E prevented and whether it reversed the growth inhibitory effect of high glucose. Methods. For the preventive experiment, rat mesangial cells (RMC) were grown in control glucose medium with the addition of 100 μM of vitamin E. High glucose (27.5 mM) was added to the medium concurrent with the vitamin E addition. The 3-(4,5-di-methylthiazol-2-yl)-2,5 diphenyltetrazolium bromide (MTT) assay was used to measure RMC proliferation. Our data confirmed the growth inhibitory effect of high glucose and showed that the growth inhibition was prevented by vitamin E. To examine whether vitamin E reversed the growth inhibitory effects of high glucose, RMC were grown in control and high glucose medium. Contrary to previous prevention type studies, vitamin E was not added to the medium until growth inhibition of the RMC by the high glucose was established. Results. Our data show that it took 5 days of vitamin E administration to reverse the growth inhibitory effect of high glucose. Conclusion. This is the first time that vitamin E has been shown to reverse this high-glucose-induced inhibition of RMC, suggesting that vitamin E reverses a potentially important pathogenetic process. Received: January 6, 1999 / Accepted: May 20, 1999     

The protective effect of vitamin E on cerebral ischemia

Using the "canine model of the completely ischemic brain regulated with a perfusion method," the effects on cerebral ischemia of vitamin E, which is known to act as an antioxidant, were investigated. After pretreatment with vitamin E by oral or intravenous administration, cerebral blood flow was reduced to 1/10th the normal state and, 1 hour later, allowed to return to normal. Subsequent changes in electrical activity were observed, and the effects of vitamin E were evaluated. In the control group, no recovery of electrical activity was seen. In the groups given vitamin E, the recovery time was significantly shortened in the dogs given 30 mg/kg of vitamin E intravenously. Furthermore, in the groups treated with vitamin E, distinct recovery of electroencephalographic potentials at 3 hours after recirculation was apparent. These effects were more favorable in the case of intravenous administration than in the case of oral administration. These experimental results indicate that the administration of vitamin E is effective in protecting the brain from cerebral ischemia.     

Effect of vitamin E on tamoxifen-treated breast cancer cells

BACKGROUND: Induction of apoptosis by tamoxifen has been postulated to involve oxidative stress. Tamoxifen (TAM) may act on estrogen receptors (ER) located in the plasma membrane. Our hypothesis that supplemental antioxidant vitamin E (alpha-tocopherol) acts at the plasma membrane to alter the effectiveness of tamoxifen was tested in ER-positive breast cancer cell lines, MCF-7 and T47D. METHODS: Cells were treated in vitro with 20-muM TAM alone and in combination with 10-muM alpha-tocopherol (AT). Estrogen growth signals were quantified by immunohistochemical staining for the mitogen-activated protein kinase p-ERK. Rapid changes in intracellular calcium were detected in TAM-treated MCF-7 and T-47D cells by fluorescence microscopy of cells loaded with the calcium-sensitive dye Fluo 4AM. Apoptosis was assayed by flow cytometry. RESULTS: Proliferating cells in normal medium exhibited strong p-ERK staining. Addition of TAM abolished p-ERK staining and caused cell rounding and death. The addition of AT led to the restoration of cell proliferation and p-ERK expression even in the presence of high-dose TAM. Intracellular calcium rapidly increased in MCF-7 and T47D cells upon exposure to TAM, followed by an increase in caspase activation and eventual apoptosis. The increase in intracellular calcium was abolished by the addition of 10muM AT to TAM, and pan-caspase staining decreased at 5 hours from 72% to 41%. CONCLUSIONS: These studies suggest that supplemental vitamin E decreases the inhibitory effect of TAM on the proliferation of ER+ breast cancer cells and eliminates the rapid rise in intracellular calcium that leads to apoptosis stimulated by TAM. The use of vitamin E acetate supplements may be inadvisable for women taking tamoxifen.     

Beneficial effects of vitamin E in sperm functions in the rat after spinal cord injury

Male infertility as a result of spinal cord injury (SCI) is associated with abnormal semen qualities including low sperm counts and poor sperm motility and morphology. Clinical studies suggest that reactive oxygen species (ROS)-related events might contribute to abnormal sperm functions after SCI. The current study examined whether impaired sperm functions after SCI can be ameliorated by an antioxidant, vitamin E. Vitamin E feeding of spinal cord transected (SCX) rats during the acute (maintenance) and chronic (restoration) phases of the injury partially preserved sperm viability and mitochondrial potential; similar effects were only seen in spinal cord contused (SCC) rats during the chronic phase. A beneficial effect of vitamin E on sperm motility, however, was only observed in SCX rats during the chronic phase of the injury. These results suggest that ROS-related events might account for some of the effects of cord injury on sperm functions, depending on the extent of injury and time postinjury. Furthermore, we found that sperm heads from SCC and SCX rats were less condensed compared to those from sham control rats. Such effects were attenuated by vitamin E, suggesting that ROS-related events may also contribute to abnormal sperm morphology after SCI. Partial restoration of male accessory gland weights in those rats fed vitamin E further suggests its beneficial effects on the functions of these glands. Conclusion: Vitamin E feeding attenuated some of the effects of spinal cord injury on sperm functions and male accessory glands in the rat. These results support a role of ROS-related events in deterioration of semen quality after cord injury. Further understanding of the underlying mechanisms for effects of vitamin E on sperm functions and male accessory glands will provide scientific rationale for the use of vitamin E or other antioxidant as therapeutic means to preserve sperm functions and semen quality in SCI men.