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Ian B Puddey - One of the best experts on this subject based on the ideXlab platform.
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Supplementation with mixed Tocopherols increases serum and blood cell γ-Tocopherol but does not alter biomarkers of platelet activation in subjects with type 2 diabetes
The American journal of clinical nutrition, 2006Co-Authors: Michael W. Clarke, Natalie C Ward, Ian B Puddey, Jonathan M. Hodgson, Kevin D CroftAbstract:BACKGROUND: Some studies have shown potential benefit of vitamin E on platelet function, but several clinical trials failed to show improved cardiovascular outcome with [alpha]-Tocopherol supplementation. [Gamma]-Tocopherol, a major dietary form of vitamin E, may have protective properties different from those of [alpha]-Tocopherol. OBJECTIVE: We compared the effects of supplementation with [alpha]-Tocopherol (500 mg) and a [Gamma]-Tocopherol-rich compound (500 mg, containing 60% [Gamma]-Tocopherol) on serum and cellular Tocopherol concentrations, urinary Tocopherol metabolite excretion, and in vivo platelet activation in subjects with type 2 diabetes. DESIGN: Fifty-eight subjects were randomly assigned to receive either 500 mg [alpha]-Tocopherol/d, 500 mg mixed Tocopherols/d, or matching placebo. Serum, erythrocyte, and platelet Tocopherol and urinary metabolite concentrations were measured at baseline and after the 6-wk intervention. Soluble CD40 ligand, urinary 11-dehydro-thromboxane B₂, serum thromboxane B₂, soluble P-selectin, and von Willebrand factor were measured as biomarkers of in vivo platelet activation. RESULTS: Serum [alpha]-Tocopherol increased with both Tocopherol treatments. Serum and cellular [Gamma]-Tocopherol increased 4-fold (P < 0.001) in the mixed Tocopherol group, whereas red blood cell [Gamma]-Tocopherol decreased significantly after [alpha]-Tocopherol supplementation. Excretion of [alpha]-carboxyethyl-hydroxychroman increased significantly after supplementation with [alpha]-Tocopherol and mixed Tocopherols. Excretion of [Gamma]-carboxyethyl-hydroxychroman increased significantly after supplementation with mixed Tocopherols and after that with [alpha]-Tocopherol, which may reflect the displacement of [Gamma]-Tocopherol by [alpha]-Tocopherol due to incorporation of the latter into lipoproteins in the liver. Neither treatment had any significant effect on markers of platelet activation. CONCLUSIONS: Supplementation with [alpha]-Tocopherol decreased red blood cell [Gamma]-Tocopherol, whereas mixed Tocopherols increased both serum [alpha]-Tocopherol and serum and cellular [Gamma]-Tocopherol. Changes in serum Tocopherol closely reflect changes in cellular concentrations of Tocopherols after supplementation.
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Evidence for the nitration of Gamma-Tocopherol in vivo: 5-nitro-Gamma-Tocopherol is elevated in the plasma of subjects with coronary heart disease.
The Biochemical journal, 2002Co-Authors: Lincoln W Morton, Natalie C Ward, Kevin D Croft, Ian B PuddeyAbstract:This study investigated the hypothesis that nitration of Gamma-Tocopherol may be an important mechanism for the detoxification of reactive nitrogen oxide species in vivo. Using liquid chromatography-tandem MS we have shown that Gamma-Tocopherol can be nitrated in vivo to form 5-nitro-Gamma-Tocopherol and that concentrations of this compound are elevated in the plasma of subjects with coronary heart disease. In addition, we demonstrate in carotid-artery atherosclerotic plaque that nitration of Gamma-Tocopherol is also evident at levels similar to that seen in the plasma of subjects with coronary heart disease.
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Evidence for the nitration of γ-Tocopherol in vivo: 5-nitro-γ-Tocopherol is elevated in the plasma of subjects with coronary heart disease
Biochemical Journal, 2002Co-Authors: Lincoln W Morton, Natalie C Ward, Kevin D Croft, Ian B PuddeyAbstract:This study investigated the hypothesis that nitration of Gamma-Tocopherol may be an important mechanism for the detoxification of reactive nitrogen oxide species in vivo. Using liquid chromatography-tandem MS we have shown that Gamma-Tocopherol can be nitrated in vivo to form 5-nitro-Gamma-Tocopherol and that concentrations of this compound are elevated in the plasma of subjects with coronary heart disease. In addition, we demonstrate in carotid-artery atherosclerotic plaque that nitration of Gamma-Tocopherol is also evident at levels similar to that seen in the plasma of subjects with coronary heart disease.
Begoña Pérez-vich - One of the best experts on this subject based on the ideXlab platform.
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Genetic basis of unstable expression of high Gamma-Tocopherol content in sunflower seeds
BMC plant biology, 2012Co-Authors: María J. García-moreno, Leonardo Velasco, José M. Fernández-martínez, Begoña Pérez-vichAbstract:Background Tocopherols are natural antioxidants with both in vivo (vitamin E) and in vitro activity. Sunflower seeds contain predominantly alpha-Tocopherol (>90% of total Tocopherols), with maximum vitamin E effect but lower in vitro antioxidant action than other Tocopherol forms such as Gamma-Tocopherol. Sunflower germplasm with stable high levels of Gamma-Tocopherol (>85%) has been developed. The trait is controlled by recessive alleles at a single locus Tph2 underlying a Gamma-Tocopherol methyltransferase (Gamma-TMT). Additionally, unstable expression of increased Gamma-Tocopherol content in the range from 5 to 85% has been reported. The objective of this research was to determine the genetic basis of unstable expression of high Gamma-Tocopherol content in sunflower seeds.
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Genetic basis of unstable expression of high Gamma-Tocopherol content in sunflower seeds
BMC Plant Biology, 2012Co-Authors: María J. García-moreno, Leonardo Velasco, José M. Fernández-martínez, Begoña Pérez-vichAbstract:Background Tocopherols are natural antioxidants with both in vivo (vitamin E) and in vitro activity. Sunflower seeds contain predominantly alpha-Tocopherol (>90% of total Tocopherols), with maximum vitamin E effect but lower in vitro antioxidant action than other Tocopherol forms such as Gamma-Tocopherol. Sunflower germplasm with stable high levels of Gamma-Tocopherol (>85%) has been developed. The trait is controlled by recessive alleles at a single locus Tph2 underlying a Gamma-Tocopherol methyltransferase (Gamma-TMT). Additionally, unstable expression of increased Gamma-Tocopherol content in the range from 5 to 85% has been reported. The objective of this research was to determine the genetic basis of unstable expression of high Gamma-Tocopherol content in sunflower seeds. Results Male sterile plants of nuclear male sterile line nmsT2100, with stable high Gamma-Tocopherol content, were crossed with plants of line IAST-1, with stable high Gamma-Tocopherol content but derived from a population that exhibited unstable expression of the trait. F_2 seeds showed continuous segregation for Gamma-Tocopherol content from 1.0 to 99.7%. Gamma-Tocopherol content in F_2 plants (average of 24 individual F_3 seeds) segregated from 59.4 to 99.4%. A genetic linkage map comprising 17 linkage groups (LGs) was constructed from this population using 109 SSR and 20 INDEL marker loci, including INDEL markers for Tocopherol biosynthesis genes. QTL analysis revealed a major QTL on LG 8 that corresponded to the Gamma-TMT Tph2 locus, which suggested that high Gamma-Tocopherol lines nmsT2100 and IAST-1 possess different alleles at this locus. Modifying genes were identified at LGs 1, 9, 14 and 16, corresponding in most cases with Gamma-TMT duplicated loci. Conclusions Unstable expression of high Gamma-Tocopherol content is produced by the effect of modifying genes on tph2 ^ a allele at the Gamma-TMT Tph2 gene. This allele is present in line IAST-1 and is different to allele tph2 present in line nmsT2100, which is not affected by modifying genes. No sequence differences at the Gamma-TMT gene were found associated to allelic unstability. Our results suggested that modifying genes are mostly epistatically interacting Gamma-TMT duplicated loci.
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Genetic and Molecular Analysis of High Gamma-Tocopherol Content in Sunflower
Crop Science, 2006Co-Authors: María J. García-moreno, Leonardo Velasco, José M. Fernández-martínez, Elsa M. Vera-ruiz, Begoña Pérez-vichAbstract:Sunflower (Helianthus annuus L.) seeds contain alpha-Tocopherol as the major Tocopherol derivative, which accounts for more than 900 g kg 21 total Tocopherols. However, four sources of high GammaTocopherol content (.850 g kg 21 ) have been developed. First studies on the lines LG-17 and T2100 concluded that the trait in both lines was determined by recessive alleles at the Tph2 locus. The objectives of the present research were (i) to conduct an allelic study on the other two lines, IAST-1 and IAST-540, (ii) to identify markers linked to the Tph2 gene, and (iii) to map this gene. Plants of T2100 were crossed with plants of the other three lines, which resulted in F1 and F2 populations with uniformly high Gamma-Tocopherol content in the seeds, indicating the presence of tph2 alleles in the four lines. Genetic mapping of the Tph2 gene was conducted with an F2 population from the cross between CAS-12, with standard Tocopherol profile, and IAST540. F2 seeds segregated following a 3 low to 1 high Gamma-Tocopherol ratio. Bulked segregant analysis identified two simple sequence repeats (SSR) markers on linkage group (LG) 8 linked to Tph2. A large linkagegroupwasconstructedbygenotypingadditionalmarkers.Tph2 mapped between markers ORS312 (3.6 cM proximal) and ORS599 (1.9 cM distal). The availability of closely linked PCR-based markers and the location of the Tph2 gene on the sunflower genetic map will be useful for marker-assisted selection and further characterization of Tocopherol biosynthesis in sunflower seeds.
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Novel variation for the Tocopherol profile in a sunflower created by mutagenesis and recombination
Plant Breeding, 2004Co-Authors: Leonardo Velasco, Begoña Pérez-vich, José M. Fernández-martínezAbstract:alpha-Tocopherol is the main Tocopherol in sunflower seeds (> 90%). Because it exerts a weak antioxidant action in vitro, its partial replacement by other Tocopherols is an important breeding objective in this crop. The objective of this research was to develop novel Tocopherol profiles in sunflower through mutagenesis and genetic recombination. Seeds of four 'Peredovik' accessions were used for chemical mutagenesis with ethyl methane sulfonate (EMS). Single-seed screening in the M2 generation resulted in two M2 seeds, derived from different M1 plants, with increased Gamma-Tocopherol contents of 19.2% and 96.7%, respectively. M3 progeny from the M2 seed with the 96.7% content bred true for high Gamma-Tocopherol content, containing more than 90% Gamma-Tocopherol. M3 progeny from the M2 seed with only 19.2% Gamma-Tocopherol segregated in a range from 0 to 84.6%. Selection for high Gamma-Tocopherol content produced an M(4 : 5) line, designated IAST-1, with a stable high concentration of Gamma-Tocopherol. Crosses between IAST-1 and T589, with an increased beta-Tocopherol content, produced F2 segregants with transgressive levels of up to 77% beta-Tocopherol or up to 68% delta-Tocopherol. Both novel Tocopherol profiles were confirmed in the F3 generation.
Orhan Aydemir - One of the best experts on this subject based on the ideXlab platform.
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Protective Effects of Vitamin E Forms (Alpha-Tocopherol, Gamma-Tocopherol and d-alpha-Tocopherol Polyethylene Glycol 1000 Succinate) on Retinal Edema During Ischemia–reperfusion Injury in the Guinea Pig Retina
International Ophthalmology, 2004Co-Authors: Orhan Aydemir, Serdal Celebi, Turgut Yilmaz, Hayrettin Yekeler, A Sahap KüknerAbstract:Purpose: The purpose of this study is to provide evidence that free radical damage is a component of retinal ischemia–reperfusion (I/R) injury, and to determine whether alpha-Tocopherol, Gamma-Tocopherol and d-alpha-Tocopherol polyethylene glycol 1000 succinate (TPGS) can protect the retina from this injury. Methods: The right eyes of 40 male guinea pigs weighing 500–600 g were used. The animals were randomly assigned to group 1 (control), group 2 (I/R), group 3 (I/R plus alpha-Tocopherol), group 4 (I/R plus Gamma-Tocopherol) and group 5 (I/R plus TPGS). Groups 3, 4 and 5 received four subcutaneous injections at six-hour intervals for total dosage of 800 IU/kg alpha-Tocopherol, 1000 IU/kg Gamma-Tocopherol and 750 IU/kg TPGS, respectively. The first dose of each substance was administered 5 minutes before retinal ischemia. Retinal ischemia was induced for 90 minutes, then followed by reperfusion for 24 hours. Injections of three substances were repeated at 6, 12 and 18 hours during reperfusion. The animals were killed at 24 hours of reperfusion. Sagittal sections of 4 μm were cut and stained with hematoxylin and eosin for light microscopic evaluation. The average thickness (edema) of the inner plexiform layer for each eye was measured in sagittal sections near the optic nerve and expressed in microns. Results: All the three substances showed statistically significant protection against the formation of retinal edema during ischemia–reperfusion injury. The mean thickness of the inner plexiform layer were 15.0, 25.44, 19.81, 21.38 and 20.88 μm in control, I/R, I/R plus alpha-Tocopherol, I/R plus Gamma-Tocopherol and I/R plus TPGS groups, respectively. The results showed that the thickness of the inner plexiform layer in group 1 (control) was significantly lower than the other groups (p
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protective effects of vitamin e forms alpha Tocopherol Gamma Tocopherol and d alpha Tocopherol polyethylene glycol 1000 succinate on retinal edema during ischemia reperfusion injury in the guinea pig retina
International Ophthalmology, 2004Co-Authors: Orhan Aydemir, Serdal Celebi, Turgut Yilmaz, Hayrettin Yekeler, şahap A KuknerAbstract:Purpose: The purpose of this study is to provide evidence that free radical damage is a component of retinal ischemia–reperfusion (I/R) injury, and to determine whether alpha-Tocopherol, Gamma-Tocopherol and d-alpha-Tocopherol polyethylene glycol 1000 succinate (TPGS) can protect the retina from this injury. Methods: The right eyes of 40 male guinea pigs weighing 500–600 g were used. The animals were randomly assigned to group 1 (control), group 2 (I/R), group 3 (I/R plus alpha-Tocopherol), group 4 (I/R plus Gamma-Tocopherol) and group 5 (I/R plus TPGS). Groups 3, 4 and 5 received four subcutaneous injections at six-hour intervals for total dosage of 800 IU/kg alpha-Tocopherol, 1000 IU/kg Gamma-Tocopherol and 750 IU/kg TPGS, respectively. The first dose of each substance was administered 5 minutes before retinal ischemia. Retinal ischemia was induced for 90 minutes, then followed by reperfusion for 24 hours. Injections of three substances were repeated at 6, 12 and 18 hours during reperfusion. The animals were killed at 24 hours of reperfusion. Sagittal sections of 4 μm were cut and stained with hematoxylin and eosin for light microscopic evaluation. The average thickness (edema) of the inner plexiform layer for each eye was measured in sagittal sections near the optic nerve and expressed in microns. Results: All the three substances showed statistically significant protection against the formation of retinal edema during ischemia–reperfusion injury. The mean thickness of the inner plexiform layer were 15.0, 25.44, 19.81, 21.38 and 20.88 μm in control, I/R, I/R plus alpha-Tocopherol, I/R plus Gamma-Tocopherol and I/R plus TPGS groups, respectively. The results showed that the thickness of the inner plexiform layer in group 1 (control) was significantly lower than the other groups (p<0.001). The inner plexiform layer was thicker in the I/R group than with I/R plus alpha-Tocopherol (p<0.001), I/R plus Gamma-Tocopherol (p<0.001) and I/R plus TPGS (p<0.01). The inner plexiform layer was not thicker in the I/R plus TPGS group than in the I/R plus alpha-Tocopherol and I/R plus Gamma-Tocopherol groups. Compared to the I/R plus alpha-Tocopherol group, the inner plexiform layer was significantly thicker in the I/R plus Gamma-Tocopherol group (p<0.01). Conclusions: The results from these experiments indicate that vitamin E forms have protective effects on the retina during retinal ischemia–reperfusion injury, but, the effects of alpha-Tocopherol and TPGS appear to be much greater than that of Gamma-Tocopherol.
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Protective effects of vitamin E forms (alpha-Tocopherol, Gamma-Tocopherol and d-alpha-Tocopherol polyethylene glycol 1000 succinate) on retinal edema during ischemia-reperfusion injury in the guinea pig retina.
International ophthalmology, 2004Co-Authors: Orhan Aydemir, Serdal Celebi, Turgut Yilmaz, Hayrettin Yekeler, A Sahap KüknerAbstract:The purpose of this study is to provide evidence that free radical damage is a component of retinal ischemia-reperfusion (I/R) injury, and to determine whether alpha-Tocopherol, Gamma-Tocopherol and d-alpha-Tocopherol polyethylene glycol 1000 succinate (TPGS) can protect the retina from this injury. The right eyes of 40 male guinea pigs weighing 500-600 g were used. The animals were randomly assigned to group 1 (control), group 2 (I/R), group 3 (I/R plus alpha-Tocopherol), group 4 (I/R plus Gamma-Tocopherol) and group 5 (I/R plus TPGS). Groups 3, 4 and 5 received four subcutaneous injections at six-hour intervals for total dosage of 800 IU/kg alpha-Tocopherol, 1000 IU/kg Gamma-Tocopherol and 750 IU/kg TPGS, respectively. The first dose of each substance was administered 5 minutes before retinal ischemia. Retinal ischemia was induced for 90 minutes, then followed by reperfusion for 24 hours. Injections of three substances were repeated at 6, 12 and 18 hours during reperfusion. The animals were killed at 24 hours of reperfusion. Sagittal sections of 4 microm were cut and stained with hematoxylin and eosin for light microscopic evaluation. The average thickness (edema) of the inner plexiform layer for each eye was measured in sagittal sections near the optic nerve and expressed in microns. All the three substances showed statistically significant protection against the formation of retinal edema during ischemia-reperfusion injury. The mean thickness of the inner plexiform layer were 15.0, 25.44, 19.81, 21.38 and 20.88 microm in control, I/R, I/R plus alpha-Tocopherol, I/R plus Gamma-Tocopherol and I/R plus TPGS groups, respectively. The results showed that the thickness of the inner plexiform layer in group 1 (control) was significantly lower than the other groups (p<0.001). The inner plexiform layer was thicker in the I/R group than with I/R plus alpha-Tocopherol (p<0.001), I/R plus Gamma-Tocopherol (p<0.001) and I/R plus TPGS (p<0.01). The inner plexiform layer was not thicker in the I/R plus TPGS group than in the I/R plus alpha-Tocopherol and I/R plus Gamma-Tocopherol groups. Compared to the I/R plus alpha-Tocopherol group, the inner plexiform layer was significantly thicker in the I/R plus Gamma-Tocopherol group (p<0.01). The results from these experiments indicate that vitamin E forms have protective effects on the retina during retinal ischemia-reperfusion injury, but, the effects of alpha-Tocopherol and TPGS appear to be much greater than that of Gamma-Tocopherol.
A Sahap Kükner - One of the best experts on this subject based on the ideXlab platform.
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Protective Effects of Vitamin E Forms (Alpha-Tocopherol, Gamma-Tocopherol and d-alpha-Tocopherol Polyethylene Glycol 1000 Succinate) on Retinal Edema During Ischemia–reperfusion Injury in the Guinea Pig Retina
International Ophthalmology, 2004Co-Authors: Orhan Aydemir, Serdal Celebi, Turgut Yilmaz, Hayrettin Yekeler, A Sahap KüknerAbstract:Purpose: The purpose of this study is to provide evidence that free radical damage is a component of retinal ischemia–reperfusion (I/R) injury, and to determine whether alpha-Tocopherol, Gamma-Tocopherol and d-alpha-Tocopherol polyethylene glycol 1000 succinate (TPGS) can protect the retina from this injury. Methods: The right eyes of 40 male guinea pigs weighing 500–600 g were used. The animals were randomly assigned to group 1 (control), group 2 (I/R), group 3 (I/R plus alpha-Tocopherol), group 4 (I/R plus Gamma-Tocopherol) and group 5 (I/R plus TPGS). Groups 3, 4 and 5 received four subcutaneous injections at six-hour intervals for total dosage of 800 IU/kg alpha-Tocopherol, 1000 IU/kg Gamma-Tocopherol and 750 IU/kg TPGS, respectively. The first dose of each substance was administered 5 minutes before retinal ischemia. Retinal ischemia was induced for 90 minutes, then followed by reperfusion for 24 hours. Injections of three substances were repeated at 6, 12 and 18 hours during reperfusion. The animals were killed at 24 hours of reperfusion. Sagittal sections of 4 μm were cut and stained with hematoxylin and eosin for light microscopic evaluation. The average thickness (edema) of the inner plexiform layer for each eye was measured in sagittal sections near the optic nerve and expressed in microns. Results: All the three substances showed statistically significant protection against the formation of retinal edema during ischemia–reperfusion injury. The mean thickness of the inner plexiform layer were 15.0, 25.44, 19.81, 21.38 and 20.88 μm in control, I/R, I/R plus alpha-Tocopherol, I/R plus Gamma-Tocopherol and I/R plus TPGS groups, respectively. The results showed that the thickness of the inner plexiform layer in group 1 (control) was significantly lower than the other groups (p
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Protective effects of vitamin E forms (alpha-Tocopherol, Gamma-Tocopherol and d-alpha-Tocopherol polyethylene glycol 1000 succinate) on retinal edema during ischemia-reperfusion injury in the guinea pig retina.
International ophthalmology, 2004Co-Authors: Orhan Aydemir, Serdal Celebi, Turgut Yilmaz, Hayrettin Yekeler, A Sahap KüknerAbstract:The purpose of this study is to provide evidence that free radical damage is a component of retinal ischemia-reperfusion (I/R) injury, and to determine whether alpha-Tocopherol, Gamma-Tocopherol and d-alpha-Tocopherol polyethylene glycol 1000 succinate (TPGS) can protect the retina from this injury. The right eyes of 40 male guinea pigs weighing 500-600 g were used. The animals were randomly assigned to group 1 (control), group 2 (I/R), group 3 (I/R plus alpha-Tocopherol), group 4 (I/R plus Gamma-Tocopherol) and group 5 (I/R plus TPGS). Groups 3, 4 and 5 received four subcutaneous injections at six-hour intervals for total dosage of 800 IU/kg alpha-Tocopherol, 1000 IU/kg Gamma-Tocopherol and 750 IU/kg TPGS, respectively. The first dose of each substance was administered 5 minutes before retinal ischemia. Retinal ischemia was induced for 90 minutes, then followed by reperfusion for 24 hours. Injections of three substances were repeated at 6, 12 and 18 hours during reperfusion. The animals were killed at 24 hours of reperfusion. Sagittal sections of 4 microm were cut and stained with hematoxylin and eosin for light microscopic evaluation. The average thickness (edema) of the inner plexiform layer for each eye was measured in sagittal sections near the optic nerve and expressed in microns. All the three substances showed statistically significant protection against the formation of retinal edema during ischemia-reperfusion injury. The mean thickness of the inner plexiform layer were 15.0, 25.44, 19.81, 21.38 and 20.88 microm in control, I/R, I/R plus alpha-Tocopherol, I/R plus Gamma-Tocopherol and I/R plus TPGS groups, respectively. The results showed that the thickness of the inner plexiform layer in group 1 (control) was significantly lower than the other groups (p<0.001). The inner plexiform layer was thicker in the I/R group than with I/R plus alpha-Tocopherol (p<0.001), I/R plus Gamma-Tocopherol (p<0.001) and I/R plus TPGS (p<0.01). The inner plexiform layer was not thicker in the I/R plus TPGS group than in the I/R plus alpha-Tocopherol and I/R plus Gamma-Tocopherol groups. Compared to the I/R plus alpha-Tocopherol group, the inner plexiform layer was significantly thicker in the I/R plus Gamma-Tocopherol group (p<0.01). The results from these experiments indicate that vitamin E forms have protective effects on the retina during retinal ischemia-reperfusion injury, but, the effects of alpha-Tocopherol and TPGS appear to be much greater than that of Gamma-Tocopherol.
Kevin D Croft - One of the best experts on this subject based on the ideXlab platform.
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Supplementation with mixed Tocopherols increases serum and blood cell γ-Tocopherol but does not alter biomarkers of platelet activation in subjects with type 2 diabetes
The American journal of clinical nutrition, 2006Co-Authors: Michael W. Clarke, Natalie C Ward, Ian B Puddey, Jonathan M. Hodgson, Kevin D CroftAbstract:BACKGROUND: Some studies have shown potential benefit of vitamin E on platelet function, but several clinical trials failed to show improved cardiovascular outcome with [alpha]-Tocopherol supplementation. [Gamma]-Tocopherol, a major dietary form of vitamin E, may have protective properties different from those of [alpha]-Tocopherol. OBJECTIVE: We compared the effects of supplementation with [alpha]-Tocopherol (500 mg) and a [Gamma]-Tocopherol-rich compound (500 mg, containing 60% [Gamma]-Tocopherol) on serum and cellular Tocopherol concentrations, urinary Tocopherol metabolite excretion, and in vivo platelet activation in subjects with type 2 diabetes. DESIGN: Fifty-eight subjects were randomly assigned to receive either 500 mg [alpha]-Tocopherol/d, 500 mg mixed Tocopherols/d, or matching placebo. Serum, erythrocyte, and platelet Tocopherol and urinary metabolite concentrations were measured at baseline and after the 6-wk intervention. Soluble CD40 ligand, urinary 11-dehydro-thromboxane B₂, serum thromboxane B₂, soluble P-selectin, and von Willebrand factor were measured as biomarkers of in vivo platelet activation. RESULTS: Serum [alpha]-Tocopherol increased with both Tocopherol treatments. Serum and cellular [Gamma]-Tocopherol increased 4-fold (P < 0.001) in the mixed Tocopherol group, whereas red blood cell [Gamma]-Tocopherol decreased significantly after [alpha]-Tocopherol supplementation. Excretion of [alpha]-carboxyethyl-hydroxychroman increased significantly after supplementation with [alpha]-Tocopherol and mixed Tocopherols. Excretion of [Gamma]-carboxyethyl-hydroxychroman increased significantly after supplementation with mixed Tocopherols and after that with [alpha]-Tocopherol, which may reflect the displacement of [Gamma]-Tocopherol by [alpha]-Tocopherol due to incorporation of the latter into lipoproteins in the liver. Neither treatment had any significant effect on markers of platelet activation. CONCLUSIONS: Supplementation with [alpha]-Tocopherol decreased red blood cell [Gamma]-Tocopherol, whereas mixed Tocopherols increased both serum [alpha]-Tocopherol and serum and cellular [Gamma]-Tocopherol. Changes in serum Tocopherol closely reflect changes in cellular concentrations of Tocopherols after supplementation.
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Evidence for the nitration of Gamma-Tocopherol in vivo: 5-nitro-Gamma-Tocopherol is elevated in the plasma of subjects with coronary heart disease.
The Biochemical journal, 2002Co-Authors: Lincoln W Morton, Natalie C Ward, Kevin D Croft, Ian B PuddeyAbstract:This study investigated the hypothesis that nitration of Gamma-Tocopherol may be an important mechanism for the detoxification of reactive nitrogen oxide species in vivo. Using liquid chromatography-tandem MS we have shown that Gamma-Tocopherol can be nitrated in vivo to form 5-nitro-Gamma-Tocopherol and that concentrations of this compound are elevated in the plasma of subjects with coronary heart disease. In addition, we demonstrate in carotid-artery atherosclerotic plaque that nitration of Gamma-Tocopherol is also evident at levels similar to that seen in the plasma of subjects with coronary heart disease.
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Evidence for the nitration of γ-Tocopherol in vivo: 5-nitro-γ-Tocopherol is elevated in the plasma of subjects with coronary heart disease
Biochemical Journal, 2002Co-Authors: Lincoln W Morton, Natalie C Ward, Kevin D Croft, Ian B PuddeyAbstract:This study investigated the hypothesis that nitration of Gamma-Tocopherol may be an important mechanism for the detoxification of reactive nitrogen oxide species in vivo. Using liquid chromatography-tandem MS we have shown that Gamma-Tocopherol can be nitrated in vivo to form 5-nitro-Gamma-Tocopherol and that concentrations of this compound are elevated in the plasma of subjects with coronary heart disease. In addition, we demonstrate in carotid-artery atherosclerotic plaque that nitration of Gamma-Tocopherol is also evident at levels similar to that seen in the plasma of subjects with coronary heart disease.
