Vitamin E refers to a family of several compounds that possess a similar chemical structure comprising a chromanol ring with a 16-carbon side chain. The degree of saturation of the side chain, and positions and nature of methyl groups designate the compounds as tocopherols ortocotrienols. Vitamin E compounds have antioxidant properties due to a hydroxyl group on the chromanol ring. Recently, it has been suggested that vitamin E may also regulate signal transduction and gene expression. We previously reported that lifelong dietary vitamin E (alpha-tocopherol) supplementation significantly increased median lifespan in C57BL/6 mice by 15%. This lifespan extension appeared to be independent of any antioxidant effect. Employing a transcriptional approach, we suggest that this increase in lifespan may reflect an anti-cancer effect via induction of the P21 signalling pathway, since cancer is the major cause of death in small rodents. We suggest that the role of this pathway in life span extension following supplementation of vitamin E now requires further investigation.
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Tocopherols and tocotrienols, collectively known as vitamin E, are essential antioxidant nutrients. The biological fates and metabolite profiles of the different forms are not clearly understood. The objective of this study is to simultaneously analyze the metabolites of different tocopherols and tocotrienols in mouse and human samples. Using HPLC/electrochemical detection and mass spectrometry, 18 tocopherol-derived and 24 tocotrienol-derived side-chain degradation metabolites were identified in fecal samples. Short-chain degradation metabolites, in particular γ- and δ- carboxyethyl hydroxychromans (CEHCs) and carboxymethylbutyl hydroxychromans (CMBHCs) were detected in urine, serum and liver samples, with tocopherols additionally detected in serum and liver samples. The metabolite profiles of tocotrienols and tocopherols were similar, but new tocotrienol metabolites with double bonds were identified. This is the first comprehensive report describing simultaneous analysis of different side-chain metabolites of tocopherols and tocotrienols in mice and humans. Urinary metabolites may serve as useful biomarkers for nutritional assessment of vitamin E.
Vitamin E is found to reverse the effects of nicotine on bone and this study aimed to determine its mechanism. Male Sprague Dawley rats were divided into four groups and treated for 3 months: Group 1 was the control group (RC). Groups 2 (N), 3 (N+TT) and 4 (N+ATF) received nicotine 7 mg/kg throughout the treatment period. In addition, groups 3 and 4 received tocotrienol 60 mg/kg and alpha-tocopherol 60 mg/kg respectively during months 2 and 3. Parameters measured were serum osteoprotegerin (OPG), serum receptor activator of nuclear factor kappa B ligand (RANKL), femoral and lumbar bone calcium content and body weight. Nicotine did not affect OPG or RANKL levels but reduced bone calcium content suggesting the calcium loss is not due to increase osteoclastogenesis. OPG was increased in N+ATF while RANKL was slightly increased in N+TT. Both vitamin E supplements restored bone calcium loss induced by nicotine. Nicotine impaired weight gain in all treatment groups starting week 4 however, N+TT group was comparable to RC from week 6 onwards. Bone protective effects of ATF, but not TT, may be partly due to inhibition of osteoclastogenesis.
Tocotrienol (T3) is an unsaturated form of natural vitamin E that has been focused on because of its potential health benefits (i.e., antioxidative, antihypercholesterolemic, and antiangiogenic effects). The presence of T3 in some plant sources (e.g., rice bran and palm oil) is known, but its distribution in other edible sources and its daily intake remain unclear. In this study, we aimed at clarifying the distribution of T3 in various food sources and estimating the daily T3 intake of Japanese population. T3 contents of 242 food items and 64 meal items were measured by using normal-phase HPLC with fluorescence detection. As for the results, T3 contents were nondetectable to 12 mg T3/kg wet wt of food items, and nondetectable to 1.3 mg T3/item of processed (cooked) meal. Accordingly, the daily intake of T3 was estimated as 1.9-2.1 mg T3/day/person. The estimated daily intake of T3 appears rather low compared with the intake of tocopherol (8-10 mg/day/person as reported in the Japanese National Nutrition Survey), and additional T3 is important for its therapeutic aspects.
BACKGROUND AND AIMS: Intake of the antioxidant vitamins C and E lowers the oxidative stress. The study aimed to determine plasma concentrations of vitamin C and tocotrienols after supplementation of both vitamins in young male adults.
MATERIALS AND METHODS: A total of 64 police recruits were randomly assigned to one of these groups: (a) 500 mg vitamin C (Vitamin C), (b) 200 mg Tocovid (Tocotrienol), (c) combination of 500 mg vitamin C and 200 mg Tocovid (Combination) or (d) placebo (Placebo) for eight-weeks of supplementation followed by six-week washout period.
RESULTS: In Combination group, mean plasma vitamin C concentration significantly increased from baseline 2.86 +/- 1.19 mg/L to 10.37 +/- 1.29 mg/L and 15.63 +/- 1.27 mg/L after four- and eight-week supplementation, respectively. The corresponding figures for alpha-, delta- and gamma-tocotrienols were 9.9 +/- 2.5 ng/ml to 104.1 +/- 19.8 ng/ml and 112.8 +/- 38.0 ng/ml; 2.5 +/- 0.9 ng/ml to 29.9 +/- 7.0 ng/ml and 17.9 +/- 4.7 ng/ml; 19.2 +/- 3.1 ng/ml to 75.2 +/- 24.1 ng/ml and 161.7 +/- 49.9 ng/ml, respectively. In Vitamin C group, plasma vitamin C concentrations were significantly increased. Conversely, concentration of plasma vitamin C in Tocotrienol group increased from baseline of 2.72 +/- 0.20 mg/L to 6.80 +/- 0.63 mg/L and 8.9 +/- 0.77 mg/L respectively. Plasma concentrations of alpha-, delta- and gamma-tocotrienols in this group were significantly elevated. After 6-week washout period, all the elevated concentrations returned to basal levels.
Vitamin E, like tocotrienols and tocopherols, is constituted of compounds essential for animal cells. Vitamin E is exclusively synthesized by photosynthetic eukaryotes and other oxygenic photosynthetic organisms such as cyanobacteria. In order to prevent lipid oxidation, the plants mainly accumulate tocochromanols in oily seeds and fruits or in young tissues undergoing active cell divisions. From a health point of view, at the moment there is a great interest in the natural forms of tocochromanols, because they are considered promising compounds able to maintain a healthy cardiovascular system and satisfactory blood cholesterol levels. Some evidence suggests that the potency of the antioxidant effects may differ between natural or synthetic source of tocochromanols (vitamin E).
Recently, vitamin E has been found to promote the bone structure of nicotine-treated rats well above their baseline values, thus suggesting that vitamin E may have some anabolic action. A bone anabolic agent acts by improving the bone structure leading to stronger bone. To assess the possible anabolic action vitamin E on bone, we supplemented alpha-tocopherol (ATF) or gamma-tocotrienol (GTT) at 60 mg/kg or vehicle [normal control (NC) group] for 4 months to normal male rats and measured their bone structure and biomechanical properties. Histomorphometric analysis revealed that vitamin E-supplemented rats have better trabecular volume, thickness, number, and separation than rats receiving vehicle only. For the first time we reported that GTT improves all the parameters of bone biomechanical strength, while ATF only improved some of the parameters compared to the NC group. Vitamin E supplementation, especially with the gamma isomer, improves bone structure, which contributed to stronger bone. Therefore, vitamin E has the potential to be used as an anabolic agent to treat osteoporosis or as bone supplements for young adults to prevent osteoporosis in later years.
Nearly after one century of research and thousands of publications, the physiological function(s) of vitamin E remain unclear. Available evidence suggests a role in cell homeostasis that occurs through the modulation of specific signaling pathways and genes involved in proliferative, metabolic, inflammatory, and antioxidant pathways. Vitamin E presence in the human body is under close metabolic control so that only alpha-tocopherol and, to a lower extent, gamma-tocopherol are retained and delivered to tissues. Other vitamin E forms that are not retained in the body in significant amounts, exhibit responses in vitro that are different form those of alpha-tocopherol and may include tumor cell specific toxicity and apoptosis. These responses provide a therapeutic potential for these minor forms, either as such or metabolically modified, to produce bioactive metabolites. These cellular effects go beyond the properties of lipophilic antioxidant attributed to alpha-tocopherol particularly investigated for its alleged protective role in atherosclerosis or other oxidative stress conditions. Understanding signaling and gene expression effects of vitamin E could help assign a physiological role to this vitamin, which will be discussed in this review. Besides vitamin E signaling, attention will be given to tocotrienolsas one of the emerging topics in vitamin E research and a critical re-examination of the most recent clinical trials will be provided together with the potential use of vitamin E in disease prevention and therapy.
A method for the determination of tocopherols and tocotrienols in vegetable oils by nanoliquid chromatography with UV-vis detection has been developed. The separation of tocopherols was optimized in terms of mobile phase composition on the basis of the best compromise between efficiency, resolution, and analysis time. The optimal conditions were achieved using a C18 silica monolithic column (150 mm x 0.1 mm) with an isocratic elution of acetonitrile/methanol/water (acidified with 0.2% acetic acid) at a flow rate of 0.5 microL min(-1), giving a total analysis time below 18 min. The method has been applied to the quantification of tocopherols and tocotrienols present in several vegetable oils with different botanical origins.