Impact of Four Week Swimming Exercise with Alpha-Tocopherol Supplementation on Fertility Potential in Healthy Rats.

Kalantari A, Saremi A, Shavandi N, Foroutan Nia A

Urol J. 2017 Aug 29;14(5):5023-5026.

Abstract

PURPOSE:

The aim of this study was to evaluate the effect of 4 week intensive swimming exercise and alpha-tocopherol supplementation on testicular oxidative stress and spermatogenesis in rats.

MATERIALS AND METHODS:

40 male rats were randomly assigned to Control (C), Sham (S), Exercise (E) and Exercise + supplement (ES) groups. Exercise training performed for 4 weeks (1session/day, 6days/week). Each session included 180 minutes of swimming. In ES group, alpha-ocopherol was injected at a dose of 50 mg/kg/day. 48 hours after last training session, all rats were killed and gonads of them were removed from their body for histological and biochemical assays. All statistical analysis was performed by SPSS 16. P values less than 0.05 were considered as statistically significant.

RESULTS:

Total testicular antioxidant capacity increased significantly in E (P = .003) and ES groups (P = .001) whereas there was no significant difference between C and E group in testicle Malondialdehyde (a lipid peroxidation marker) level (P = .999) and spermatogenesis quality (P = .381). Testicle Malondialdehyde level decreased (P = .009) and spermatogenesis quality was improved significantly in ES group (P = .001).

CONCLUSION:

Alpha-tocopherol supplementation is effective in order to improve spermatogenesis process in athletes who exercise with high intensity.

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Comparison between tocotrienol and omeprazole on gastric growth factors in stress-exposed rats.

Nur Azlina MF, Qodriyah HMS, Chua KH, Kamisah Y

World J Gastroenterol. 2017 Aug 28;23(32):5887-5894. doi: 10.3748/wjg.v23.i32.5887.

Abstract

AIM:

To investigate and compare the effects of tocotrienol and omeprazole on gastric growth factors in rats exposed to water-immersion restraint stress (WIRS).

METHODS:

Twenty-eight male Wistar rats were randomly assigned to four groups of seven rats. The two control groups were administered vitamin-free palm oil (vehicle) and the two treatment groups were given omeprazole (20 mg/kg) or tocotrienol (60 mg/kg) by oral gavage. After 28 d of treatment, rats from one control group and both treated groups were subjected to WIRS one time for 3.5 h. Gastric lesions were measured and gastric tissues were obtained to measure vascular endothelial growth factor (VEGF), epidermal growth factor (EGF), basic fibroblast growth factor (bFGF), and transforming growth factor-alpha (TGF-α) mRNA expression.

RESULTS:

Rats exposed to WIRS for 3.5 h demonstrated the presence of considerable ulcers in the form of gastric erosion. The lesion index in the stressed control (S) group was increased (P < 0.001) compared to the tocotrienol treated and omeprazole treated groups. Stress led to a decrease in gastric VEGF (P < 0.001), bFGF (P < 0.001) and TGF-α (P < 0.001) mRNA levels and caused an increase in EGF mRNA (P < 0.001) that was statistically significant compared to the non-stressed control group. Although both treatment agents exerted similar ulcer reducing ability, only treatment with tocotrienol led to increased expression of VEGF (P = 0.008), bFGF (P = 0.001) and TGF-α (P = 0.002) mRNA.

CONCLUSION:

Tocotrienol provides gastroprotective effects in WIRS-induced ulcers. Compared to omeprazole, tocotrienol exerts a similar protective effect, albeit through multiple mechanisms of protection, particularly through up-regulation of growth factors that assist in repair of gastric tissue injuries.

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Vitamin E deficiency may lead to increased colorectal cancer risk: Chinese meta-analysis

Vitamin E deficiency might be linked to an increased risk of colorectal cancer, according to a Chinese systematic review and meta-analysis. The review concluded that while serum vitamin E deficiency might be associated with a higher risk of developing colorectal cancer, ”necessary prospective cohort studies should be conducted to assess the effect of vitamin E” on the risk of colorectal cancer.

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Study: Vitamin E supplementation may decrease muscle injury

Can oral ingestion of vitamin E help reduce muscle fiber damage? Yes, according to a group of researchers in Brazil… in mice at least.

The use of antioxidant as a therapeutic agent has recently gained renewed interest”, wrote the researchers from the State University of Campinas of Sao Paolo, Brazil. ”Several studies have demonstrated positive outcomes regarding some diseases such as cardiovascular disease, atherosclerosis, allergic disease, neuromuscular disease,  and muscular dystrophies.”

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Gamma-tocotrienol profoundly alters sphingolipids in cancer cells by inhibition of dihydroceramide desaturase and possibly activation of sphingolipid hydrolysis during prolonged treatment.

Jang Y, Rao X, Jiang Q

J Nutr Biochem. 2017 Aug;46:49-56. doi: 10.1016/j.jnutbio.2017.04.003. Epub 2017 Apr 12.

Abstract

Vitamin E gamma-tocotrienol (γTE) is known to have anticancer effects, but mechanisms underlying these actions are not clear. Here using liquid chromatography tandem mass spectrometry, we show that γTE induced marked changes of sphingolipids including rapid elevation of dihydrosphingosine and dihydroceramides (dhCers) in various types of cancer cells. The elevation of dihydrosphingolipids coincided with increased cellular stress, as indicated by JNK phosphorylation, and was prior to any sign of induction of apoptosis. Chemically blocking de novo synthesis of sphingolipids partially counteracted γTE-induced apoptosis and autophagy. Experiments using 13C315N-labeled l-serine together with enzyme assays indicate that γTE inhibited cellular dihydroceramide desaturase (DEGS) activity without affecting its protein expression or de novo synthesis of sphingolipids. Unlike the effect on dhCers, γTE decreased ceramides (Cers) after 8-h treatment but increased C18:0-Cer and C16:0-Cer after 16 and 24 h, respectively. The increase of Cers coincides with γTE-induced apoptosis and autophagy. Since γTE inhibits DEGS and decreases de novo Cer synthesis, elevation of Cers during prolonged γTE treatment is likely caused by sphingomeylinase-mediated hydrolysis of sphingomyelin. This idea is supported by the observation that an acid sphingomeylinase inhibitor partially reversed γTE-induced cell death. Our study demonstrates that γTE altered sphingolipid metabolism by inhibiting DEGS activity and possibly by activating SM hydrolysis during prolonged treatment in cancer cells.

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Tocotrienols for bone health: a translational approach.

Shen CL, Klein A, Chin KY, Mo H, Tsai P, Yang RS, Chyu MC, Ima-Nirwana S

Ann N Y Acad Sci. 2017 Aug;1401(1):150-165. doi: 10.1111/nyas.13449.

Abstract

Osteoporosis, a degenerative bone disease, is characterized by low bone mass and microstructural deterioration of bone tissue resulting in aggravated bone fragility and susceptibility to fractures. The trend of extended life expectancy is accompanied by a rise in the prevalence of osteoporosis and concomitant complications in the elderly population. Epidemiological evidence has shown an association between vitamin E consumption and the prevention of age-related bone loss in elderly women and men. Animal studies show that ingestion of vitamin E, especially tocotrienols, may benefit bone health in terms of maintaining higher bone mineral density and improving bone microstructure and quality. The beneficial effects of tocotrienols on bone health appear to be mediated via antioxidant/anti-inflammatory pathways and/or 3-hydroxy-3-methylglutaryl coenzyme A mechanisms. We discuss (1) an overview of the prevalence and etiology of osteoporosis, (2) types of vitamin E (tocopherols versus tocotrienols), (3) findings of tocotrienols and bone health from published in vitro and animal studies, (4) possible mechanisms involved in bone protection, and (5) challenges and future direction for research.

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Excessive Vitamin E Intake Does Not Cause Bone Loss in Male or Ovariectomized Female Mice Fed Normal or High-Fat Diets.

Ikegami H, Kawawa R, Ichi I, Ishikawa T, Koike T, Aoki Y, Fujiwara Y

J Nutr. 2017 Aug 23. pii: jn248575. doi: 10.3945/jn.117.248575. [Epub ahead of print]

Abstract

Background: Animal studies on the effects of vitamin E on bone health have yielded conflicting and inconclusive results, and to our knowledge, no studies have addressed the effect of vitamin E on bone in animals consuming a high-fat diet (HFD).Objective: This study aimed to evaluate the effect of excessive vitamin E on bone metabolism in normal male mice and ovariectomized female mice fed a normal diet (ND) or HFD.Methods: In the first 2 experiments, 7-wk-old male mice were fed an ND (16% energy from fat) containing 75 (control), 0 (vitamin E-free), or 1000 (high vitamin E) mg vitamin E/kg (experiment 1) or an HFD (46% energy from fat) containing 0, 200, 500, or 1000 mg vitamin E/kg (experiment 2) for 18 wk. In the third experiment, 7-wk-old sham-operated or ovariectomized female mice were fed the ND (75 mg vitamin E/kg) or HFD containing 0 or 1000 mg vitamin E/kg for 8 wk. At the end of the feeding period, blood and femurs were collected to measure bone turnover markers and analyze histology and microcomputed tomography.Results: In experiments 1 and 2, vitamin E intake had no effect on plasma alkaline phosphatase (ALP), tartrate-resistant acid phosphatase (TRAP) activity, or bone formation, resorption, or volume in femurs in mice fed the ND or HFDs. In experiment 3, bone volume was significantly reduced (85%) in ovariectomized mice compared with that in sham-operated mice (P < 0.05), but it did not differ among mice fed the 3 diets. Plasma ALP and TRAP activities and bone formation and resorption in femur were similar among ovariectomized mice fed the HFD containing 0 or 1000 mg vitamin E/kg.Conclusions: The results suggest that excess vitamin E intake does not cause bone loss in normal male mice or in ovariectomized or sham-operated female mice, regardless of dietary fat content.

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Do low-serum vitamin E levels increase the risk of Alzheimer disease in older people? Evidence from a meta-analysis of case-control studies.

Dong Y, Chen X, Liu Y, Shu Y, Chen T, Xu L, Li M, Guan X

Int J Geriatr Psychiatry. 2017 Aug 23. doi: 10.1002/gps.4780. [Epub ahead of print]

Abstract

OBJECTIVE:

Whether low-serum vitamin E increases the risk of Alzheimer disease (AD) in older people remains inconclusive. This meta-analysis aims to synthesize evidence-based case-control studies to evaluate the association between serum vitamin E and the risk of AD.

METHODS:

Potentially relevant studies were selected through PubMed, Embase, Wanfang, Chongqing VIP, and China National Knowledge Infrastructure databases by using the core terms Vitamin E/alpha-tocopherol and Alzheime’s disease/senile dementia/AD in the titles, abstracts, and keywords of the articles. The association between serum vitamin E levels and AD was estimated by using the weighted mean difference (WMD) and 95% confidence interval by adopting a random effects model. Heterogeneity was assessed by using Cochran Q test and I2 statistic. Forest plot was used to present the results graphically from meta-analysis. Publication bias was evaluated by using funnel plots and Egger test.

RESULTS:

We identified 17 studies that met the eligibility criteria. The studies included 2057 subjects with 904 AD patients and 1153 controls. The results indicated that AD patients had a lower concentration of serum vitamin E compared with healthy controls among older people (WMD = -6.811 μmol/L, 95% confidence interval -8.998 to -4.625; Z = -6.105, P < .001). Publication bias was not detected and sensitivity analysis performed by omitting each study, and calculating the pooled WMD again for the remaining studies indicated the results stable.

CONCLUSIONS:

Alzheimer disease is associated with a low concentration of serum vitamin E in older people. However, necessary prospective cohort studies should be conducted to determine the risk of serum vitamin E for AD in the future.

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Lack of antioxidants increases obesity risk in sleep-deprived men: Korean study

Low dietary antioxidant intake — coupled with insufficient sleep — could lead to an increased risk of obesity in men, a Korean study has found. The study noted that ”a combined effect of the consumption of dietary antioxidant vitamins, such as vitamin A, retinol, carotene, vitamin C, and vitamin E, on sleep duration was observed with respect to the odds of being obese.

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What the Brain Craves – Omega-3s, Vitamin E and Vitamin D

Many nutrients really are “food for thought.” The brain is the most active part of the body and has an enormous appetite, requiring about 20 percent of our total energy intake to function. But energy is not the sole source of “food” for the brain: vitamins, fatty acids and minerals are also important for optimizing cognitive health. The high energy demands and the considerable blood flow to the brain mean that nutrients involved in energy metabolism and producing healthy blood cells will help us maintain normal cognition, such as the B-vitamins and iron. Other micronutrients play an unappreciated role in brain health: omega-3s, vitamin E and vitamin D. How do they contribute to nutrition for the brain?

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