Blog Archives

Effect of palm-based tocotrienols and tocopherol mixture supplementation on platelet aggregation in subjects with metabolic syndrome: a randomised controlled trial.

Gan YL, Fu JY, Lai OM, Chew BH, Yuen KH, Teng KT, Nesaretnam K, Selvaduray KR, Meganathan P

Sci Rep. 2017 Sep 14;7(1):11542. doi: 10.1038/s41598-017-11813-w.

Abstract

Tocotrienols, the unsaturated form of vitamin E, were reported to modulate platelet aggregation and thrombotic mechanisms in pre-clinical studies. Using a Food and Drug Administration (FDA)-approved cartridge-based measurement system, a randomised, double-blind, crossover and placebo-controlled trial involving 32 metabolic syndrome adults was conducted to investigate the effect of palm-based tocotrienols and tocopherol (PTT) mixture supplementation on platelet aggregation reactivity. The participants were supplemented with 200 mg (69% tocotrienols and 31% α-tocopherol) twice daily of PTT mixture or placebo capsules for 14 days in a random order. After 14 days, each intervention was accompanied by a postprandial study, in which participants consumed 200 mg PTT mixture or placebo capsule after a meal. Blood samples were collected on day 0, day 14 and during postprandial for the measurement of platelet aggregation reactivity. Subjects went through a 15-day washout period before commencement of subsequent intervention. Fasting platelet aggregation reactivity stimulated with adenosine diphosphate (ADP) did not show substantial changes after supplementation with PTT mixture compared to placebo (p = 0.393). Concomitantly, changes in postprandial platelet aggregation reactivity remained similar between PTT mixture and placebo interventions (p = 0.408). The results of this study highlight the lack of inhibitory effect on platelet aggregation after short-term supplementation of PTT mixture in participants with metabolic syndrome.

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This little-known vitamin may lower your stroke risk – The STAR

Numerous studies show that a little-known type of vitamin E called tocotrienols can protect the brain against stroke damage and reduce the risk of recurrent stroke. According to tocotrienol researcher Prof Chandan K. Sen, brain damage during a stroke can be prevented by triggering the surrounding blood vessels to dilate and redirect the blood flow around a blockage. The blood vessel “redirect” is the result of 10 weeks worth of supplementation with palm tocotrienols in a canine-stroke model study.

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The Ameliorative Effects of a Tocotrienol-Rich Fraction on the AGE-RAGE Axis and Hypertension in High-Fat-Diet-Fed Rats with Metabolic Syndrome.

Cheng HS, Ton SH, Tan JBL, Abdul Kadir K

Nutrients. 2017 Sep 7;9(9). pii: E984. doi: 10.3390/nu9090984.

Abstract

The clinical value of tocotrienols is increasingly appreciated because of the unique therapeutic effects that are not shared by tocopherols. However, their effect on metabolic syndrome is not well-established. This study aimed to investigate the effects of a tocotrienol-rich fraction (TRF) from palm oil in high-fat-diet-treated rats. Male, post-weaning Sprague Dawley rats were provided high-fat (60% kcal) diet for eight weeks followed by a TRF (60 mg/kg) treatment for another four weeks. Physical, metabolic, and histological changes were compared to those on control and high-fat diets respectively. High-fat feeding for eight weeks induced all hallmarks of metabolic syndrome. The TRF reversed systolic and diastolic hypertension, hypercholesterolemia, hepatic steatosis, impaired antioxidant defense, and myeloperoxidase hyperactivity triggered by the high-fat diet. It also conferred an inhibitory effect on protein glycation to reduce glycated hemoglobin A1c and advanced glycation end products (AGE). This was accompanied by the suppression of the receptor for advanced glycation end product (RAGE) expression in the liver. The treatment effects on visceral adiposity, glycemic control, triglyceride level, as well as peroxisome proliferator-activated receptor α and γ expression were negligible. To conclude, treatment with a TRF exhibited protective effects on the cardiovascular and liver health in addition to the amelioration of plasma redox imbalance and AGE-RAGE activation. Further investigation as a therapy for metabolic syndrome is therefore worthwhile.

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Vitamin E isoform γ-tocotrienol protects against emphysema in cigarette smoke-induced COPD.

Peh HY, Tan WSD, Chan TK, Pow CW, Foster PS, Wong WSF.

Free Radic Biol Med. 2017 Sep;110:332-344. doi: 10.1016/j.freeradbiomed.2017.06.023. Epub 2017 Jul 3.

Abstract

Inflammation and oxidative stress contribute to emphysema in COPD. Although corticosteroids are the standard of care for COPD, they do not reduce oxidative stress, and a subset of patients is steroid-resistant. Vitamin E isoform γ-tocotrienol possesses both anti-inflammatory and anti-oxidative properties that may protect against emphysema. We aimed to establish the therapeutic potential of γ-tocotrienol in cigarette smoke-induced COPD models in comparison with prednisolone. BALB/c mice were exposed to cigarette smoke for 2 weeks or 2 months. γ-Tocotrienol and prednisolone were given orally. Bronchoalveolar lavage (BAL) fluid and lung tissues were assessed for inflammation, oxidative damage, and regulation of transcription factor activities. Emphysema and lung function were also evaluated. γ-Tocotrienol dose-dependently reduced cigarette smoke-induced BAL fluid neutrophil counts and levels of cytokines, chemokines and oxidative damage biomarkers, and pulmonary pro-inflammatory and pro-oxidant gene expression, but restored lung endogenous antioxidant activities. γ-Tocotrienol acted by inhibiting nuclear translocation of STAT3 and NF-κB, and up-regulating Nrf2 activation in the lungs. In mice exposed to 2-month cigarette smoke, γ-tocotrienol ameliorated bronchial epithelium thickening and destruction of alveolar sacs in lungs, and improved lung functions. In comparison with prednisolone, γ-tocotrienol demonstrated better anti-oxidative efficacy, and protection against emphysema and lung function in COPD. We revealed for the first time the anti-inflammatory and antioxidant efficacies of γ-tocotrienol in cigarette smoke-induced COPD models. In addition, γ-tocotrienol was able to attenuate emphysematous lesions and improve lung function in COPD. γ-Tocotrienol may have therapeutic potential for the treatment of COPD.

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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 13C3, 15N-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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