The 40-year gap between the discoveries of tocopherols and tocotrienols means the former gets a lot more attention, according to American River Nutrition founder Dr. Barrie Tan.
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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.
Inhibition of rapid delayed rectifier potassium current (IKr) by ischemia/reperfusion and its recovery by vitamin E in ventricular myocytes.
Chen Y, Yin C, Yang Y, Fan Z, Shang J, Tan W.
J Electrocardiol. 2017 Jul - Aug;50(4):437-443. doi: 10.1016/j.jelectrocard.2017.03.007. Epub 2017 Mar 14.
Abstract
Ischemia/reperfusion (I/R) induces prolongation of QT interval and action potential duration (APD), which is a major cardiac electrical disorder in patients with arrhythmias. However, the mechanism of QT interval prolongation induced by I/R remains unclear. In the present study, we hypothesized that the rapid component of delayed rectifier potassium (IKr) channel plays an important role in I/R-induced QT interval prolongation. We observed a marked attenuation of IKr and a significant prolongation of action potential duration (APD) in a simulated I/R system with sodium dithionite (Na2S2O4) in ventricular myocytes of guinea pigs. The IKr current density was inhibited by 64% and APD increased by 87% respectively. Moreover, the inhibition of IKr is primarily ascribed to overproduction of reactive oxygen species (ROS) by I/R, which can be partly reversed by antioxidant vitamin E (100μmol/L). The value of IKr tail current density increased from 0.516±0.040 pA/pF in I/R to 0.939±0.091 pA/pF when treated with vitamin E. Moreover, we also demonstrated that QTc interval was increased by I/R and reversed by Vitamin E in isolated guinea pig hearts. In conclusion, the inhibition of IKr is one of the underlying mechanisms of prolongation of QT interval and APD in I/R. Vitamin E might have a benefit in coronary reperfusion therapy.
Palm oil vitamin E exports set to surge with discovery of major health benefits – New Straits Times
SEPANG: Malaysia’s annual RM70 million palm oil vitamin E exports to the global pharmaceutical industry are set to expand, as medical studies show that it lowers bad cholesterol levels, kills cancer cells and protects our brain against the debilitating effects of a stroke.
“As more medical studies (discover) the benefits of palm oil vitamin E, the future is bright for mankind,” said Plantation Industries and Commodities Minister Datuk Seri Mah Siew Keong.
“Malaysia’s Health Ministry has just released its sampling study on the country’s 30 million population consuming palm oil in their daily diet. The results affirmed that consuming palm oil doesn’t have any adverse effect on our heart’s health,” he said.
Tocopherol source may affect breast milk vitamin E profile, says study
The vitamin E alpha-tocopherol is imperative to a baby’s nervous system development, and they primarily get this from breast milk or formula. In a clinical trial, researchers from Abbott Nutrition found that there might be a difference in how synthetic versus natural alpha-tocopherols reach an infant.
The Response of Macro- and Micronutrient Nutrient Status and Biochemical Processes in Rats Fed on a Diet with Selenium-Enriched Defatted Rapeseed and/or Vitamin E Supplementation.
Rýdlová M, Růnová K, Száková J, Fučíková A, Hakenová A, Mlejnek P, Zídek V, Tremlová J, Mestek O, Kaňa A, Zídková J, Melčová M, Truhlářová K, Tlustoš P.
Biomed Res Int. 2017;2017:6759810. doi: 10.1155/2017/6759810. Epub 2017 May 30.
Abstract
The response of nutrient status and biochemical processes in (i) Wistar and (ii) spontaneously hypertensive (SHR) rats upon dietary intake of selenium- (Se-) enriched defatted rapeseed (DRS) and/or vitamin E fortification was examined to assess the health benefit of DRS in animal nutrition. Twenty-four individuals of each type of rat were used: The control group was fed with an untreated diet (Diet A). In Diets B and C, soybean meal was replaced with defatted DRS, which comprised 14% of the total diet. The selenized DRS application resulted in ~3-fold increase of Se content in the diet. Diet C was also fortified with the addition of vitamin E, increasing the natural content by 30%. The Se content of the blood and kidneys tended to increase in the DRS groups, where the changes were significant (P < 0.05) only in the case of SHR rats. The iodine (I) content and the proportion of iodide in rat livers indicated a lower transformation rate of iodide into organoiodine compounds compared to the control. Slight and ambiguous alterations in the antioxidative response of the rat were observed in the DRS groups, but the addition of vitamin E to the diet helped to moderate these effects.
Inhibition of rapid delayed rectifier potassium current (IKr) by ischemia/reperfusion and its recovery by vitamin E in ventricular myocytes.
Chen Y, Yin C, Yang Y, Fan Z, Shang J, Tan W.
J Electrocardiol. 2017 Jul - Aug;50(4):437-443. doi: 10.1016/j.jelectrocard.2017.03.007. Epub 2017 Mar 14.
Abstract
Ischemia/reperfusion (I/R) induces prolongation of QT interval and action potential duration (APD), which is a major cardiac electrical disorder in patients with arrhythmias. However, the mechanism of QT interval prolongation induced by I/R remains unclear. In the present study, we hypothesized that the rapid component of delayed rectifier potassium (IKr) channel plays an important role in I/R-induced QT interval prolongation. We observed a marked attenuation of IKr and a significant prolongation of action potential duration (APD) in a simulated I/R system with sodium dithionite (Na2S2O4) in ventricular myocytes of guinea pigs. The IKr current density was inhibited by 64% and APD increased by 87% respectively. Moreover, the inhibition of IKr is primarily ascribed to overproduction of reactive oxygen species (ROS) by I/R, which can be partly reversed by antioxidant vitamin E (100μmol/L). The value of IKr tail current density increased from 0.516±0.040 pA/pF in I/R to 0.939±0.091 pA/pF when treated with vitamin E. Moreover, we also demonstrated that QTc interval was increased by I/R and reversed by Vitamin E in isolated guinea pig hearts. In conclusion, the inhibition of IKr is one of the underlying mechanisms of prolongation of QT interval and APD in I/R. Vitamin E might have a benefit in coronary reperfusion therapy.
Vitamin E-deficient embryos are cognitively impaired even after diet improves
Zebrafish deficient in vitamin E produce offspring beset by behavioral impairment and metabolic problems, new research at Oregon State University shows.
The findings are important because the neurological development of zebrafish is similar to that of humans, and nutrition surveys indicate roughly 95 percent of women in the U.S. have inadequate intakes of this critical micronutrient.
The problem may be exacerbated in women of child-bearing age who avoid high-fat foods and may not have a diet rich in oils, nuts and seeds, which are among the foods with the highest levels of vitamin E, an antioxidant necessary for normal embryonic development in vertebrates.
How to Cure Sleep Apnea: 4 Non-CPAP Remedies
Untreated or poorly treated sleep apnea leaves you tired all the time and suffering from excessive daytime sleepiness and other sleep apnea symptoms. Use of the continuous positive airway pressure device or CPAP mask has been the gold standard of cures for sleep apnea over the past 25 years. But because of the discomfort of wearing the device, 20 to 50 percent of those who try it cannot tolerate this sleep apnea cure. Fortunately there are alternative ways for how to cure sleep apnea.
The effect of tocopheryl phosphates (TPM) on the development of atherosclerosis in apolipoprotein-e deficient mice.
Libinaki R, Vinh A, Tesanovic-Klajic S, Widdop RE, Gaspari TA.
Clin Exp Pharmacol Physiol. 2017 Jul 26. doi: 10.1111/1440-1681.12821. [Epub ahead of print]
Abstract
α-Tocopheryl phosphate (TP) is a naturally occurring form of Vitamin E found in the body. In the present study we compared the ability of an α-TP mixture (TPM) against a standard Vitamin E supplement, α-tocopherol acetate (TA) on the development of atherosclerotic lesions in ApoE-deficient mice. Mice were maintained on either a normal chow diet for 24 weeks (Normal Diet), versus a group in which the final 8 weeks of the 24 week period mice were placed on a high fat (21%), high cholesterol (0.15%) challenge diet (HFHC), to exacerbate atherosclerotic lesion development.. The difference in these two control groups established the extent of the diet induced atherosclerotic lesion development. Mice in the various treatment groups received either TA (300mg/kg chow) or TPM (6.7 to 200mg/kg chow) for 24 weeks, with TPM treatment resulting in dose-dependent significant reductions in atherosclerotic lesion formation and plasma levels of pro-inflammatory cytokines. TA-treated mice, with the tocopherol equivalent TPM dose (200mg/kg chow), showed no significant reduction in plasma lipid levels or evidence for aortic lesion regression. At this TPM equivalent TA dose, a 44% reduction in aortic lesion formation was observed. In addition, these TPM treated mice, also showed a marked reduction in aortic superoxide formation and decreased circulating plasma levels of known pro-inflammatory markers IL-6, MCP-1, IL-1β, IFN-γ and TNF-α. These findings indicate that TPM treatment slows progression of atherosclerotic lesions in ApoE-deficient mice with this effect potentially involving reduced oxidative stress and decreased inflammation.