Alpha and Gamma Tocopherols in Cerebrospinal Fluid and Serum from Older, Male, Human Subjects

Vatassery, Govind T.; Adityanjee,; Quach, Hung T.; Smith, William E.; Kuskowski, Michael A.; Melnyk, Dean

doi:10.1080/07315724.2004.10719366

Cited by 32 publications

(24 citation statements)

References 26 publications

(28 reference statements)

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“…The concentration of α-T was estimated to be 42.1 ± 17.0 nM in human cerebrospinal fluid, while the concentration of other vitamin E components is much lower, e.g., γ-tocopherol concentration was found to be 5.9 ± 2.8 nM [11]. This is consistent with data of other earlier studies [12,13].…”

Section: Introductionsupporting

confidence: 87%

α-Tocopherol at Nanomolar Concentration Protects PC12 Cells from Hydrogen Peroxide-Induced Death and Modulates Protein Kinase Activities

Захарова

Sokolova²,

Bayunova³

et al. 2012

IJMS

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The aim of this work was to compare protective and anti-apoptotic effects of α-tocopherol at nanomolar and micromolar concentrations against 0.2 mM H2O2-induced toxicity in the PC12 neuronal cell line and to reveal protein kinases that contribute to α-tocopherol protective action. The protection by 100 nM α-tocopherol against H2O2-induced PC12 cell death was pronounced if the time of pre-incubation with α-tocopherol was 3–18 h. For the first time, the protective effect of α-tocopherol was shown to depend on its concentration in the nanomolar range (1 nM < 10 nM < 100 nM), if the pre-incubation time was 18 h. Nanomolar and micromolar α-tocopherol decreased the number of PC12 cells in late apoptosis induced by H2O2 to the same extent if pre-incubation time was 18 h. Immunoblotting data showed that α-tocopherol markedly diminished the time of maximal activation of extracellular signal-regulated kinase 1/2 (ERK 1/2) and protein kinase B (Akt)-induced in PC12 cells by H2O2. Inhibitors of MEK 1/2, PI 3-kinase and protein kinase C (PKC) diminished the protective effect of α-tocopherol against H2O2-initiated toxicity if the pre-incubation time was long. The modulation of ERK 1/2, Akt and PKC activities appears to participate in the protection by α-tocopherol against H2O2-induced death of PC12 cells. The data obtained suggest that inhibition by α-tocopherol in late stage ERK 1/2 and Akt activation induced by H2O2 in PC12 cells makes contribution to its protective effect, while total inhibition of these enzymes is not protective.

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Section: Introductionsupporting

confidence: 87%

α-Tocopherol at Nanomolar Concentration Protects PC12 Cells from Hydrogen Peroxide-Induced Death and Modulates Protein Kinase Activities

Захарова

Sokolova²,

Bayunova³

et al. 2012

IJMS

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“…Thus, α-tocopherol, and γ-tocopherol, which are at elevated levels in olive oil (widely used in the Mediterranean diet), and which can cross the blood brain barrier [51,52], could be useful to attenuate the toxic effects of 7KC on microglial cells, which are thought to contribute to neurodegeneration. By analogy with DHA, which is a fatty acid, it is of interest to determine whether oleic acid (the major fatty acid of olive oil) is able to prevent 7KC-induced cellular dysfunction.…”

Section: Introductionmentioning

confidence: 99%

“…Vitamin E is a fat-soluble vitamin which covers a set of eight organic molecules, four tocopherols (α-, β-, γ-, and δ-tocopherol) and four tocotrienols (α-, β-, γ-, and δ-tocotrienol). Some of the compounds studied (α-tocopherol, γ-tocopherol, OA), which are known to pass the blood brain barrier [51,52], are major components of olive oil, which is widely used in the Mediterranean diet. The ability of α-tocopherol, γ-tocopherol, Trolox, and OA to prevent the toxic effects of 7KC, especially their ability to impair 7KC-induced mitochondrial and peroxisomal dysfunction, was therefore evaluated in BV-2 cells.…”

Section: Introductionmentioning

confidence: 99%

Protective Effects of α-Tocopherol, γ-Tocopherol and Oleic Acid, Three Compounds of Olive Oils, and No Effect of Trolox, on 7-Ketocholesterol-Induced Mitochondrial and Peroxisomal Dysfunction in Microglial BV-2 Cells

Debbabi

Nury

Zarrouk

et al. 2016

IJMS

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Lipid peroxidation products, such as 7-ketocholesterol (7KC), may be increased in the body fluids and tissues of patients with neurodegenerative diseases and trigger microglial dysfunction involved in neurodegeneration. It is therefore important to identify synthetic and natural molecules able to impair the toxic effects of 7KC. We determined the impact of 7KC on murine microglial BV-2 cells, especially its ability to trigger mitochondrial and peroxisomal dysfunction, and evaluated the protective effects of α- and γ-tocopherol, Trolox, and oleic acid (OA). Multiple complementary chemical assays, flow cytometric and biochemical methods were used to evaluate the antioxidant and cytoprotective properties of these molecules. According to various complementary assays to estimate antioxidant activity, only α-, and γ-tocopherol, and Trolox had antioxidant properties. However, only α-tocopherol, γ-tocopherol and OA were able to impair 7KC-induced loss of mitochondrial transmembrane potential, which is associated with increased permeability to propidium iodide, an indicator of cell death. In addition, α-and γ-tocopherol, and OA were able to prevent the decrease in Abcd3 protein levels, which allows the measurement of peroxisomal mass, and in mRNA levels of Abcd1 and Abcd2, which encode for two transporters involved in peroxisomal β-oxidation. Thus, 7KC-induced side effects are associated with mitochondrial and peroxisomal dysfunction which can be inversed by natural compounds, thus supporting the hypothesis that the composition of the diet can act on the function of organelles involved in neurodegenerative diseases.

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“…These results are in line with previous report [10] where long-term incubation with 10 and 100 nM α-T before induction of oxidative stress led to a signifi cant increase in the number of survived neurons in rat brain cortex. In addition, a small but signifi cant improvement of viability of PC12 cells [1] or cortical neurons [10] can be noted as soon as after α-T concentration in the spinal fl uid and subsequently in the intercellular space of brain is 42.1±17.0 nM [12]. This highlights the importance of investigation of effects and mechanism of action of physiological nanomolar α-T concentrations, which affect neurons of human and animal brain from outside in vivo, but such studies are so far solitary and fragmentary [1,10].…”

Section: Resultsmentioning

confidence: 97%

α-Tocopherol Prevents ERK1/2 Activation in PC12 Cells under Conditions of Oxidative Stress and Its Contribution to the Protective Effect

2013

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Preincubation with 100 nM and 100 μM α-tocopherol for 18 h prevented long-term activation of extracellular signal-activated kinase (ERK1/2), induced by H2O2in PC12 cells. α-Tocopherol significantly reduced H2O2-induced death of PC12 cell, but its protective effect was significantly lower in the presence of ERK1/2 inhibitor. These data show that prevention of long-term activation of ERK1/2 by α-tocopherol contributes to the increase in viability of PC12 cells exposed to H2O2. This fact suggests that inhibition of ERK1/2 activity by α-tocopherol reduces neuronal cell death in the brain under conditions of oxidative stress in vivo.

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Alpha and Gamma Tocopherols in Cerebrospinal Fluid and Serum from Older, Male, Human Subjects

Cited by 32 publications

References 26 publications

α-Tocopherol at Nanomolar Concentration Protects PC12 Cells from Hydrogen Peroxide-Induced Death and Modulates Protein Kinase Activities

α-Tocopherol at Nanomolar Concentration Protects PC12 Cells from Hydrogen Peroxide-Induced Death and Modulates Protein Kinase Activities

Protective Effects of α-Tocopherol, γ-Tocopherol and Oleic Acid, Three Compounds of Olive Oils, and No Effect of Trolox, on 7-Ketocholesterol-Induced Mitochondrial and Peroxisomal Dysfunction in Microglial BV-2 Cells

α-Tocopherol Prevents ERK1/2 Activation in PC12 Cells under Conditions of Oxidative Stress and Its Contribution to the Protective Effect

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