DL-alpha-TocopherolCAS# 59-02-9 |
- DL-α-Tocopherol
Catalog No.:BCN9040
CAS No.:10191-41-0
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 59-02-9 | SDF | Download SDF |
PubChem ID | 14985 | Appearance | Oil |
Formula | C29H50O2 | M.Wt | 430.7 |
Type of Compound | Phenols | Storage | Desiccate at -20°C |
Solubility | DMSO : ≥ 100 mg/mL (232.17 mM) *"≥" means soluble, but saturation unknown. | ||
Chemical Name | (2R)-2,5,7,8-tetramethyl-2-[(4R,8R)-4,8,12-trimethyltridecyl]-3,4-dihydrochromen-6-ol | ||
SMILES | CC1=C(C(=C2CCC(OC2=C1C)(C)CCCC(C)CCCC(C)CCCC(C)C)C)O | ||
Standard InChIKey | GVJHHUAWPYXKBD-IEOSBIPESA-N | ||
Standard InChI | InChI=1S/C29H50O2/c1-20(2)12-9-13-21(3)14-10-15-22(4)16-11-18-29(8)19-17-26-25(7)27(30)23(5)24(6)28(26)31-29/h20-22,30H,9-19H2,1-8H3/t21-,22-,29-/m1/s1 | ||
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. |
Description | DL-alpha-tocopherol, a potent inhibitor of phorbol ester induced shape change of erythro- and megakaryoblastic leukemia cells. DL-alpha-tocopherol acetate protects endothelial cell membranes from oxidative damage and disruption and limits the magnitude of haemorrhage and its spread from the subependyma into the ventricles; it also protects human skin fibroblasts against the cytotoxic effect of UVB, and its mechanism seems to be related to inhibition of UV-induced lipid peroxidation or to the antioxidation effect of dl-alpha-tocopherol. |
Targets | PKC |
In vitro | Protective effect of dl-alpha-tocopherol on the cytotoxicity of ultraviolet B against human skin fibroblasts in vitro.[Pubmed: 2076374]Photodermatol Photoimmunol Photomed. 1990 Aug;7(4):173-7.The effect of DL-alpha-Tocopherol on ultraviolet light, 280-320 nm (UVB)-induced damage of human skin fibroblasts was studied by measuring the colony-forming ability, unscheduled DNA synthesis (UDS) and malondialdehyde (MDA) production. |
In vivo | Effect of antioxidant therapy with dl-alpha-tocopherol on cardiovascular structure in experimental renal failure.[Pubmed: 12164869]Kidney Int. 2002 Sep;62(3):877-84.
Protective effect of vitamin E (DL-alpha-tocopherol) against intraventricular haemorrhage in premature babies.[Pubmed: 6407714 ]Br Med J (Clin Res Ed). 1983 Jul 9;287(6385):81-4.
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Kinase Assay | dl-alpha-tocopherol, a potent inhibitor of phorbol ester induced shape change of erythro- and megakaryoblastic leukemia cells.[Pubmed: 9284955]Dl-α-tocopherol enhances the herbicide 1,1'-dimetyl-4,4'-bipyridium dichloride (paraquat, PQ) genotoxicity in cultured anuran leukocytes.[Pubmed: 22150823]Hereditas. 2011 Nov;148(4-5):118-24.
J Cell Physiol. 1997 Sep;172(3):351-60.Synthetic vitamin E, DL-alpha-Tocopherol, added to a human erythroleukemia HEL and a megakaryoblastic leukemia, Meg-01, cell culture produced potent dose-dependent inhibition of phorbol ester-induced adhesion and of the morphologic changes accompanying it. |
Structure Identification | Carbohydr Polym. 2013 Jan 30;92(1):856-64.Self-assembled nanoparticles of modified-chitosan conjugates for the sustained release of DL-α-tocopherol.[Pubmed: 23218376]
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DL-alpha-Tocopherol Dilution Calculator
DL-alpha-Tocopherol Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 2.3218 mL | 11.609 mL | 23.218 mL | 46.436 mL | 58.045 mL |
5 mM | 0.4644 mL | 2.3218 mL | 4.6436 mL | 9.2872 mL | 11.609 mL |
10 mM | 0.2322 mL | 1.1609 mL | 2.3218 mL | 4.6436 mL | 5.8045 mL |
50 mM | 0.0464 mL | 0.2322 mL | 0.4644 mL | 0.9287 mL | 1.1609 mL |
100 mM | 0.0232 mL | 0.1161 mL | 0.2322 mL | 0.4644 mL | 0.5805 mL |
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. |
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Self-assembled nanoparticles of modified-chitosan conjugates for the sustained release of DL-alpha-tocopherol.[Pubmed:23218376]
Carbohydr Polym. 2013 Jan 30;92(1):856-64.
Synthetic O6-succinylated chitosan and commercial glycol chitosan were covalently linked to dl-alpha-tocopheryl monoesters for controlled release of vitamin E. These conjugates formed self-assembled nanoparticles in aqueous solution with 254-496 nm mean diameters and DL-alpha-Tocopherol contents between 27 and 39% (w/w). The particles appeared as 40-75 nm almost spherical nanoparticles when studied by scanning and transmission electron microscopy upon drying. Drug linking to chitosan matrix was confirmed by FTIR spectroscopy and proton NMR. Conjugates were also characterized by differential scanning calorimetry and wide-angle X-ray diffraction. In vitro tocopherol release studies performed in water at acid pH indicated a drug release dependence on drug content, hydrated particle sizes and employed chitosan derivative. Almost constant release rates were observed the first 7h. The obtained nanoparticles exhibited radical scavenging activity in DPPH essay. The potential of these nanoparticles was also demonstrated by the enhancement of HMVEC cell proliferation.
Effect of antioxidant therapy with dl-alpha-tocopherol on cardiovascular structure in experimental renal failure.[Pubmed:12164869]
Kidney Int. 2002 Sep;62(3):877-84.
BACKGROUND: Chronic renal failure is characterized by remodeling of the structure of the heart and the vasculature, for example, left ventricular hypertrophy, myocardial fibrosis, capillary/myocyte mismatch, as well as thickening of intramyocardial arteries and of peripheral arteries and veins. Furthermore, uremia is a state of increased oxygen stress. It was the purpose of this study to examine whether these findings are interrelated. METHODS: To investigate whether antioxidative therapy with DL-alpha-Tocopherol (Toco; vitamin E) interferes with the development of abnormal cardiovascular structure in experimental renal failure, 28 male Sprague-Dawley rats were subjected to partial renal ablation (subtotal nephrectomy, SNX) or to sham operation (sham). SNX were either left untreated or received the antioxidant Toco (2 x 1500 IE/kg BW/week in the pellets). Blood pressure was measured using tail plethysmography. The experiment was terminated after 12 weeks. Heart and left ventricular weight were determined and the following parameters were measured using morphometry and stereology: volume densities of cardiomyocytes, capillaries and non-vascular interstitium; length density and total length of cardiac capillaries, wall thickness of intramyocardial arterioles and of the aorta. RESULTS: Systolic blood pressure and body weight were comparable in all groups. Treatment with Toco led to significantly increased plasma concentrations of Toco. Left ventricular weight and wall thickness of intramyocardial arteries were significantly higher in both SNX groups compared to sham controls. Volume density of the cardiac interstitial tissue was significantly higher in untreated SNX than in Toco treated SNX and sham control rats. Length density of capillaries was significantly lower in untreated SNX than in control rats; however, the values were significantly higher, and even higher than in sham controls, when SNX were treated with Toco. CONCLUSIONS: Treatment with the antioxidant DL-alpha-Tocopherol prevented cardiomyocyte/capillary mismatch, and to some extent also myocardial fibrosis in rats with renal failure. The results point to a role of oxidative stress in the genesis of myocardial interstitial fibrosis and capillary deficit of the heart.
Dl-alpha-tocopherol enhances the herbicide 1,1'-dimetyl-4,4'-bipyridium dichloride (paraquat, PQ) genotoxicity in cultured anuran leukocytes.[Pubmed:22150823]
Hereditas. 2011 Nov;148(4-5):118-24.
This cytogenetic and pharmacological study attempts to clarify genotoxicity-enhancement-effect of DL-alpha-Tocopherol (one form of vitamin E) in combination with the herbicide 1,1'-dimetyl-4,4'-bipyridium dichloride (paraquat, PQ) on cultured anuran leukocytes using the superoxide dismutase-mimic Mn(III)tetrakis(1-methyl-4-pyridyl)porphyrin (Mn(III)TMpyP), the hydrogen peroxide-scavenger catalase and the electron donor nicotinamide adenine dinucleotido phosphate (NADPH). PQ only was found to induce structural chromosomal damage in cultured anuran leukocytes in a dose-dependent manner. PQ plus NADPH, which served as positive control, enhanced the genotoxic effect of PQ. DL-alpha-Tocopherol only did not induce any structural chromosomal damage in the leukocytes. PQ plus DL-alpha-Tocopherol, however, enhanced the genotoxic effect of PQ. PQ plus Mn(III)TMpyP, PQ plus catalase and PQ plus Mn(III)TMpyP plus catalse suppressed the genotoxic effect of PQ. Furthermore, PQ plus DL-alpha-Tocopherol-enhanced chromosomal damage was also inhibited by Mn(III)TMpyP plus catalase. These results suggest that DL-alpha-Tocopherol in combination with PQ functions as an electron donor to PQ.
dl-alpha-tocopherol, a potent inhibitor of phorbol ester induced shape change of erythro- and megakaryoblastic leukemia cells.[Pubmed:9284955]
J Cell Physiol. 1997 Sep;172(3):351-60.
Synthetic vitamin E, DL-alpha-Tocopherol, added to a human erythroleukemia HEL and a megakaryoblastic leukemia, Meg-01, cell culture produced potent dose-dependent inhibition of phorbol ester-induced adhesion and of the morphologic changes accompanying it. The inhibition was reversible by withdrawal of supplemental vitamin E from the medium. DL-alpha-Tocopherol also inhibited protein kinase C activity both at baseline and after phorbol ester stimulation. Arachidonic acid stimulated protein kinase C activity of erythroleukemia cells and promoted their adhesion, an effect that was also inhibited by DL-alpha-Tocopherol. Introduction of a protein kinase C-neutralizing antibody or a protein kinase C-inhibitor substrate into permeabilized HEL cells inhibited phorbol ester-induced adhesion and shape change. DL-alpha-Tocopherol also affected the cellular distribution of protein kinase C, shifting the major portion of the enzyme to the cytosol fraction and reducing phorbol ester-induced membrane association of the enzyme. Thus, protein kinase C appears to mediate shape change and adhesion, both of which are strongly inhibited by DL-alpha-Tocopherol.
Protective effect of dl-alpha-tocopherol on the cytotoxicity of ultraviolet B against human skin fibroblasts in vitro.[Pubmed:2076374]
Photodermatol Photoimmunol Photomed. 1990 Aug;7(4):173-7.
The effect of DL-alpha-Tocopherol on ultraviolet light, 280-320 nm (UVB)-induced damage of human skin fibroblasts was studied by measuring the colony-forming ability, unscheduled DNA synthesis (UDS) and malondialdehyde (MDA) production. Regarding the cell toxicity, the values of the mean lethal dose (D0) of UV in fibroblast strains from 5 normal subjects were examined. D0 increased dose-dependently when the cells were cultured in the presence of DL-alpha-Tocopherol at the concentration of 10-1000 micrograms/ml. UDS induced by 500 J/m2 UVB irradiation was not altered by treatment of 100 micrograms/ml DL-alpha-Tocopherol. MDA did not increase after 500 J/m2 UVB irradiation in the fibroblasts cultured with 100 micrograms/ml DL-alpha-Tocopherol, while MDA in the fibroblasts cultured without DL-alpha-Tocopherol increased after irradiation. These results suggest that DL-alpha-Tocopherol protects human skin fibroblasts against the cytotoxic effect of UVB, and its mechanism seems to be related to inhibition of UV-induced lipid peroxidation or to the antioxidation effect of DL-alpha-Tocopherol.
Protective effect of vitamin E (DL-alpha-tocopherol) against intraventricular haemorrhage in premature babies.[Pubmed:6407714]
Br Med J (Clin Res Ed). 1983 Jul 9;287(6385):81-4.
Forty four babies, of less than 32 weeks' gestation, were either randomly given 25 mg/kg vitamin E (DL-alpha-Tocopherol acetate) intramuscularly after birth (day 0) and on days 1, 2, and 3 or served as controls. Frequent real time ultrasound examinations of the brain were made in each baby during the first week and less frequently thereafter. In babies under 32 weeks' gestation the incidence of intraventricular haemorrhage was lower in supplemented babies (18.8%) compared with the controls (56.3%). On days 0, 1, 2, and 3 median plasma vitamin E concentrations in babies without haemorrhage and in those with subependymal haemorrhage only were similar. Babies with intraventricular haemorrhage had lower median concentrations on day 1 (p less than 0.002) and day 2 (p less than 0.05) compared with those with subependymal haemorrhage and lower concentrations on day 0 (p less than 0.02) and day 1 (p less than 0.05) compared with those without haemorrhage. These findings suggest that in premature babies vitamin E, an antioxidant, protects endothelial cell membranes from oxidative damage and disruption and limits the magnitude of haemorrhage and its spread from the subependyma into the ventricles.