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    DL-alpha-Tocopherol
    DL-alpha-Tocopherol
    Information
    CAS No. 59-02-9 Price $30 / 20mg
    Catalog No.CFN90041Purity>=98%
    Molecular Weight430.7Type of CompoundPhenols
    FormulaC29H50O2Physical DescriptionOil
    Download COA    MSDS    SDF    ManualSimilar structuralComparison (Web)  (SDF)
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    DL-alpha-Tocopherol

    DL-alpha-Tocopherol
    Product Name DL-alpha-Tocopherol
    CAS No.: 59-02-9
    Catalog No.: CFN90041
    Molecular Formula: C29H50O2
    Molecular Weight: 430.7 g/mol
    Purity: >=98%
    Type of Compound: Phenols
    Physical Desc.: Oil
    Targets: PKC
    Source: The herbs of Isodon adenantha
    Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
    Price: $30 / 20mg
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    Similar structural: Comparison (Web)  (SDF)
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  • Related Screening Libraries
    Size /Price /Stock 10 mM * 100 uL in DMSO / Inquiry / In-stock
    10 mM * 1 mL in DMSO / Inquiry / In-stock
    Related Libraries
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  • Biological Activity
    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:
    Photodermatol Photoimmunol Photomed. 1990 Aug;7(4):173-7.
    Protective effect of dl-alpha-tocopherol on the cytotoxicity of ultraviolet B against human skin fibroblasts in vitro.[Pubmed: 2076374]
    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.
    METHODS AND RESULTS:
    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.
    CONCLUSIONS:
    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.
    In vivo:
    Kidney Int. 2002 Sep;62(3):877-84.
    Effect of antioxidant therapy with dl-alpha-tocopherol on cardiovascular structure in experimental renal failure.[Pubmed: 12164869]

    METHODS AND RESULTS:
    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. 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.
    Br Med J (Clin Res Ed). 1983 Jul 9;287(6385):81-4.
    Protective effect of vitamin E (DL-alpha-tocopherol) against intraventricular haemorrhage in premature babies.[Pubmed: 6407714 ]

    METHODS AND RESULTS:
    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.
    CONCLUSIONS:
    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.
    DL-alpha-Tocopherol Description
    Source: The herbs of Isodon adenantha
    Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
    Storage: Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

    Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

    Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com

    After receiving: The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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    Calculate Dilution Ratios(Only for Reference)
    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 need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
    Protocol
    Kinase Assay:
    Hereditas. 2011 Nov;148(4-5):118-24.
    Dl-α-tocopherol enhances the herbicide 1,1'-dimetyl-4,4'-bipyridium dichloride (paraquat, PQ) genotoxicity in cultured anuran leukocytes.[Pubmed: 22150823]

    METHODS AND RESULTS:
    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).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. Furthermore, PQ plus DL-alpha-Tocopherol-enhanced chromosomal damage was also inhibited by Mn(III)TMpyP plus catalase.
    CONCLUSIONS:
    These results suggest that DL-alpha-Tocopherol in combination with PQ functions as an electron donor to PQ.
    J Cell Physiol. 1997 Sep;172(3):351-60.
    dl-alpha-tocopherol, a potent inhibitor of phorbol ester induced shape change of erythro- and megakaryoblastic leukemia cells.[Pubmed: 9284955]
    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.
    METHODS AND RESULTS:
    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.
    CONCLUSIONS:
    Thus, protein kinase C appears to mediate shape change and adhesion, both of which are strongly inhibited by DL-alpha-Tocopherol.
    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]

    METHODS AND RESULTS:
    Synthetic O6-succinylated chitosan and commercial glycol chitosan were covalently linked to dl-α-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.
    CONCLUSIONS:
    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.
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