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Thierry Durand - One of the best experts on this subject based on the ideXlab platform.
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circulating 4 f4t Neuroprostane and 10 f4t Neuroprostane are related to mecp2 gene mutation and natural history in rett syndrome
International Journal of Molecular Sciences, 2021Co-Authors: Cinzia Signorini, Thierry Durand, Camille Oger, Jean-marie Galano, Valerie Bultelponce, Alexandre Guy, Silvia Leoncini, Jetty Chungyung Lee, Lucia Ciccoli, Joussef HayekAbstract:Neuroprostanes, a family of non-enzymatic metabolites of the docosahexaenoic acid, have been suggested as potential biomarkers for neurological diseases. Objective biological markers are strongly needed in Rett syndrome (RTT), which is a progressive X-linked neurodevelopmental disorder that is mainly caused by mutations in the methyl-CpG binding protein 2 (MECP2) gene with a predominant multisystemic phenotype. The aim of the study is to assess a possible association between MECP2 mutations or RTT disease progression and plasma levels of 4(RS)-4-F4t-Neuroprostane (4-F4t-NeuroP) and 10(RS)-10-F4t-Neuroprostane (10-F4t-NeuroP) in typical RTT patients with proven MECP2 gene mutation. Clinical severity and disease progression were assessed using the Rett clinical severity scale (RCSS) in n = 77 RTT patients. The 4-F4t-NeuroP and 10-F4t-NeuroP molecules were totally synthesized and used to identify the contents of the plasma of the patients. Neuroprostane levels were related to MECP2 mutation category (i.e., early truncating, gene deletion, late truncating, and missense), specific hotspot mutations (i.e., R106W, R133C, R168X, R255X, R270X, R294X, R306C, and T158M), and disease stage (II through IV). Circulating 4-F4t-NeuroP and 10-F4t-NeuroP were significantly related to (i) the type of MECP2 mutations where higher levels were associated to gene deletions (p ≤ 0.001); (ii) severity of common hotspot MECP2 mutation (large deletions, R168X, R255X, and R270X); (iii) disease stage, where higher concentrations were observed at stage II (p ≤ 0.002); and (iv) deficiency in walking (p ≤ 0.0003). This study indicates the biological significance of 4-F4t-NeuroP and 10-F4t-NeuroP as promising molecules to mark the disease progression and potentially gauge genotype-phenotype associations in RTT.
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total synthesis of a docosahexaenoic acid prostanoid using an intramolecular organocatalytic michael reaction of a formyl enal derivative
Organic Letters, 2020Co-Authors: Johanna Revolcavalier, Thierry Durand, Camille Oger, Valerie Bultelponce, Alexandre Guy, Jean-marie GalanoAbstract:The total synthesis of a docosahexaenoic-acid-derived prostaglandin, 4,11-diepi-4-F4t-Neuroprostane, featuring a complex lateral chain was achieved for the first time. A novel prostaglandin cyclope...
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nonenzymatic oxygenated metabolite of docosahexaenoic acid 4 rs 4 f4t Neuroprostane acts as a bioactive lipid molecule in neuronal cells
FEBS Letters, 2020Co-Authors: Jean-marie Galano, Camille Oger, Ho Hang Leung, Laurence Balas, Thierry DurandAbstract:Docosahexaenoic acid (DHA), an abundant fatty acid in the brain, is susceptible to auto-oxidation in situ and releases metabolites such as F4 -Neuroprostane (4-F4t -NeuroP). The presence of 4-F4t -NeuroP in the brain is not well explored. In this study, 4-F4t -NeuroP was introduced into neuroblastoma cells (SH-SY5Y) and, by in vivo infusion, into rodents. Targeted lipidomic analysis of liver and brain tissues shows significant elevation of anti-inflammatory hydroxylated DHA metabolites and an isomer of neuroprotectin D1, suggesting potential beneficial bioactivities of 4-F4t -NeuroP. Additionally, 4-F4t -NeuroP treatment in SH-SY5Y cells and primary neuronal culture consistently upregulates the transcriptional level of the antioxidant enzyme heme oxygenase-1, but the effect is reduced when 4-F4t -NeuroP is further oxidized. Our data suggest that 4-F4t -NeuroP could be neuroprotective in the native state but may have disadvantageous bioactivity when oxidized extensively.
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relevance of 4 f4t Neuroprostane and 10 f4t Neuroprostane to neurological diseases
Free Radical Biology and Medicine, 2018Co-Authors: Cinzia Signorini, Thierry Durand, Camille Oger, Jean-marie Galano, Silvia Leoncini, Lucia Ciccoli, Claudio De Felice, Marisa Carone, Monica Ulivelli, Caterina MannaAbstract:Abstract F4-Neuroprostanes (F4-NeuroPs) are non-enzymatic oxidized products derived from docosahexaenoic acid (DHA) and are suggested to be oxidative damage biomarkers of neurological diseases. However, 128 isomers can be formed from DHA oxidation and among them, 4(RS)−4-F4t-NeuroP (4-F4t-NeuroP) and 10(RS)−10-F4t-NeuroP (10-F4t-NeuroP) are the most studied. Here, we report the identification and the clinical relevance of 4-F4t-NeuroP and 10-F4t-NeuroP in plasma of four different neurological diseases, including multiple sclerosis (MS), autism spectrum disorders (ASD), Rett syndrome (RTT), and Down syndrome (DS). The identification and the optimization of the method were carried out by gas chromatography/negative-ion chemical ionization tandem mass spectrometry (GC/NICI-MS/MS) using chemically synthesized 4-F4t-NeuroP and 10-F4t-NeuroP standards and in oxidized DHA liposome. Both 4-F4t-NeuroP and 10-F4t-NeuroP were detectable in all plasma samples from MS (n = 16), DS (n = 16), ASD (n = 9) and RTT (n = 20) patients. While plasma 10-F4t-NeuroP content was significantly higher in patients of all diseases as compared to age and gender matched healthy control subjects (n = 61), 4-F4t-NeuroP levels were significantly higher in MS and RTT as compared to healthy controls. Significant positive relationships were observed between relative disease severity and 4-F4t-NeuroP levels (r = 0.469, P Overall, by comparing the different types of disease, our plasma data indicates that 4-F4t-NeuroP and 10-F4t -NeuroP: i) are biologically synthesized in vivo and circulated, ii) are related to clinical severity of neurological diseases, iii) are useful to identify shared pathogenetic pathways in distinct brain diseases, and iv) appears to be distinctive for different neurological conditions, thus representing potentially new biological disease markers. Our data strongly suggest that in vivo DHA oxidation follows preferential chemical rearrangements according to different brain diseases.
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Snapshot situation of oxidative degradation of the nervous system, kidney, and adrenal glands biomarkers-Neuroprostane and dihomo-isoprostanes-urinary biomarkers from infancy to elderly adults
Redox Biology, 2017Co-Authors: Libia Alejandra García-flores, Thierry Durand, Camille Oger, Jean-marie Galano, Sonia Medina, Federico Ferreres, Pedro Martínez-hernández, Teresa Casas-pina, Angel Gil-izquierdoAbstract:We analyzed biomarkers of lipid peroxidation of the nervous system -F2-dihomo-isoprostanes, F3-Neuroprostanes, and F4-Neuroprostanes- in urine samples from 158 healthy volunteers ranging from 4 to 88 years old with the aim of analyzing possible associations between their excretion values and age (years). Ten biomarkers were screened in the urine samples by UHPLC-QqQ-MS/MS. Four F2-dihomo-isoprostanes (ent−7-(R)−7-F2t-dihomo-isoprostane, ent−7-epi−7-F2t-dihomo-isoprostane, 17-F2t-dihomo-isoprostane, 17-epi−17-F2t-dihomo-isoprostane), and one DPA-Neuroprostane (4-F3t-Neuroprostane) were detected in the samples. On the one hand, we found a significant, positive correlation (Rho: 0.197, P=0.015) between the age increase and the amount of total F2-dihomo-IsoPs. On the other hand, the values were significantly higher in the childhood group (4–12 years old), when compared to the adolescence group (13–17 years old) and the young adult group (18–35 years old). Surprisingly, no significant differences were found between the middle-aged adults (36–64 years old) and the elderly adults (65–88 years old). We display a snapshot situation of excretory values of oxidative stress biomarkers of the nervous system, using healthy volunteers representative of the different stages of human growth and development. The values reported in this study could be used as a basal or starting point in clinical interventions related to aging processes and/or pathologies associated with the nervous system.
Jean-marie Galano - One of the best experts on this subject based on the ideXlab platform.
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circulating 4 f4t Neuroprostane and 10 f4t Neuroprostane are related to mecp2 gene mutation and natural history in rett syndrome
International Journal of Molecular Sciences, 2021Co-Authors: Cinzia Signorini, Thierry Durand, Camille Oger, Jean-marie Galano, Valerie Bultelponce, Alexandre Guy, Silvia Leoncini, Jetty Chungyung Lee, Lucia Ciccoli, Joussef HayekAbstract:Neuroprostanes, a family of non-enzymatic metabolites of the docosahexaenoic acid, have been suggested as potential biomarkers for neurological diseases. Objective biological markers are strongly needed in Rett syndrome (RTT), which is a progressive X-linked neurodevelopmental disorder that is mainly caused by mutations in the methyl-CpG binding protein 2 (MECP2) gene with a predominant multisystemic phenotype. The aim of the study is to assess a possible association between MECP2 mutations or RTT disease progression and plasma levels of 4(RS)-4-F4t-Neuroprostane (4-F4t-NeuroP) and 10(RS)-10-F4t-Neuroprostane (10-F4t-NeuroP) in typical RTT patients with proven MECP2 gene mutation. Clinical severity and disease progression were assessed using the Rett clinical severity scale (RCSS) in n = 77 RTT patients. The 4-F4t-NeuroP and 10-F4t-NeuroP molecules were totally synthesized and used to identify the contents of the plasma of the patients. Neuroprostane levels were related to MECP2 mutation category (i.e., early truncating, gene deletion, late truncating, and missense), specific hotspot mutations (i.e., R106W, R133C, R168X, R255X, R270X, R294X, R306C, and T158M), and disease stage (II through IV). Circulating 4-F4t-NeuroP and 10-F4t-NeuroP were significantly related to (i) the type of MECP2 mutations where higher levels were associated to gene deletions (p ≤ 0.001); (ii) severity of common hotspot MECP2 mutation (large deletions, R168X, R255X, and R270X); (iii) disease stage, where higher concentrations were observed at stage II (p ≤ 0.002); and (iv) deficiency in walking (p ≤ 0.0003). This study indicates the biological significance of 4-F4t-NeuroP and 10-F4t-NeuroP as promising molecules to mark the disease progression and potentially gauge genotype-phenotype associations in RTT.
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total synthesis of a docosahexaenoic acid prostanoid using an intramolecular organocatalytic michael reaction of a formyl enal derivative
Organic Letters, 2020Co-Authors: Johanna Revolcavalier, Thierry Durand, Camille Oger, Valerie Bultelponce, Alexandre Guy, Jean-marie GalanoAbstract:The total synthesis of a docosahexaenoic-acid-derived prostaglandin, 4,11-diepi-4-F4t-Neuroprostane, featuring a complex lateral chain was achieved for the first time. A novel prostaglandin cyclope...
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nonenzymatic oxygenated metabolite of docosahexaenoic acid 4 rs 4 f4t Neuroprostane acts as a bioactive lipid molecule in neuronal cells
FEBS Letters, 2020Co-Authors: Jean-marie Galano, Camille Oger, Ho Hang Leung, Laurence Balas, Thierry DurandAbstract:Docosahexaenoic acid (DHA), an abundant fatty acid in the brain, is susceptible to auto-oxidation in situ and releases metabolites such as F4 -Neuroprostane (4-F4t -NeuroP). The presence of 4-F4t -NeuroP in the brain is not well explored. In this study, 4-F4t -NeuroP was introduced into neuroblastoma cells (SH-SY5Y) and, by in vivo infusion, into rodents. Targeted lipidomic analysis of liver and brain tissues shows significant elevation of anti-inflammatory hydroxylated DHA metabolites and an isomer of neuroprotectin D1, suggesting potential beneficial bioactivities of 4-F4t -NeuroP. Additionally, 4-F4t -NeuroP treatment in SH-SY5Y cells and primary neuronal culture consistently upregulates the transcriptional level of the antioxidant enzyme heme oxygenase-1, but the effect is reduced when 4-F4t -NeuroP is further oxidized. Our data suggest that 4-F4t -NeuroP could be neuroprotective in the native state but may have disadvantageous bioactivity when oxidized extensively.
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relevance of 4 f4t Neuroprostane and 10 f4t Neuroprostane to neurological diseases
Free Radical Biology and Medicine, 2018Co-Authors: Cinzia Signorini, Thierry Durand, Camille Oger, Jean-marie Galano, Silvia Leoncini, Lucia Ciccoli, Claudio De Felice, Marisa Carone, Monica Ulivelli, Caterina MannaAbstract:Abstract F4-Neuroprostanes (F4-NeuroPs) are non-enzymatic oxidized products derived from docosahexaenoic acid (DHA) and are suggested to be oxidative damage biomarkers of neurological diseases. However, 128 isomers can be formed from DHA oxidation and among them, 4(RS)−4-F4t-NeuroP (4-F4t-NeuroP) and 10(RS)−10-F4t-NeuroP (10-F4t-NeuroP) are the most studied. Here, we report the identification and the clinical relevance of 4-F4t-NeuroP and 10-F4t-NeuroP in plasma of four different neurological diseases, including multiple sclerosis (MS), autism spectrum disorders (ASD), Rett syndrome (RTT), and Down syndrome (DS). The identification and the optimization of the method were carried out by gas chromatography/negative-ion chemical ionization tandem mass spectrometry (GC/NICI-MS/MS) using chemically synthesized 4-F4t-NeuroP and 10-F4t-NeuroP standards and in oxidized DHA liposome. Both 4-F4t-NeuroP and 10-F4t-NeuroP were detectable in all plasma samples from MS (n = 16), DS (n = 16), ASD (n = 9) and RTT (n = 20) patients. While plasma 10-F4t-NeuroP content was significantly higher in patients of all diseases as compared to age and gender matched healthy control subjects (n = 61), 4-F4t-NeuroP levels were significantly higher in MS and RTT as compared to healthy controls. Significant positive relationships were observed between relative disease severity and 4-F4t-NeuroP levels (r = 0.469, P Overall, by comparing the different types of disease, our plasma data indicates that 4-F4t-NeuroP and 10-F4t -NeuroP: i) are biologically synthesized in vivo and circulated, ii) are related to clinical severity of neurological diseases, iii) are useful to identify shared pathogenetic pathways in distinct brain diseases, and iv) appears to be distinctive for different neurological conditions, thus representing potentially new biological disease markers. Our data strongly suggest that in vivo DHA oxidation follows preferential chemical rearrangements according to different brain diseases.
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Snapshot situation of oxidative degradation of the nervous system, kidney, and adrenal glands biomarkers-Neuroprostane and dihomo-isoprostanes-urinary biomarkers from infancy to elderly adults
Redox Biology, 2017Co-Authors: Libia Alejandra García-flores, Thierry Durand, Camille Oger, Jean-marie Galano, Sonia Medina, Federico Ferreres, Pedro Martínez-hernández, Teresa Casas-pina, Angel Gil-izquierdoAbstract:We analyzed biomarkers of lipid peroxidation of the nervous system -F2-dihomo-isoprostanes, F3-Neuroprostanes, and F4-Neuroprostanes- in urine samples from 158 healthy volunteers ranging from 4 to 88 years old with the aim of analyzing possible associations between their excretion values and age (years). Ten biomarkers were screened in the urine samples by UHPLC-QqQ-MS/MS. Four F2-dihomo-isoprostanes (ent−7-(R)−7-F2t-dihomo-isoprostane, ent−7-epi−7-F2t-dihomo-isoprostane, 17-F2t-dihomo-isoprostane, 17-epi−17-F2t-dihomo-isoprostane), and one DPA-Neuroprostane (4-F3t-Neuroprostane) were detected in the samples. On the one hand, we found a significant, positive correlation (Rho: 0.197, P=0.015) between the age increase and the amount of total F2-dihomo-IsoPs. On the other hand, the values were significantly higher in the childhood group (4–12 years old), when compared to the adolescence group (13–17 years old) and the young adult group (18–35 years old). Surprisingly, no significant differences were found between the middle-aged adults (36–64 years old) and the elderly adults (65–88 years old). We display a snapshot situation of excretory values of oxidative stress biomarkers of the nervous system, using healthy volunteers representative of the different stages of human growth and development. The values reported in this study could be used as a basal or starting point in clinical interventions related to aging processes and/or pathologies associated with the nervous system.
Camille Oger - One of the best experts on this subject based on the ideXlab platform.
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circulating 4 f4t Neuroprostane and 10 f4t Neuroprostane are related to mecp2 gene mutation and natural history in rett syndrome
International Journal of Molecular Sciences, 2021Co-Authors: Cinzia Signorini, Thierry Durand, Camille Oger, Jean-marie Galano, Valerie Bultelponce, Alexandre Guy, Silvia Leoncini, Jetty Chungyung Lee, Lucia Ciccoli, Joussef HayekAbstract:Neuroprostanes, a family of non-enzymatic metabolites of the docosahexaenoic acid, have been suggested as potential biomarkers for neurological diseases. Objective biological markers are strongly needed in Rett syndrome (RTT), which is a progressive X-linked neurodevelopmental disorder that is mainly caused by mutations in the methyl-CpG binding protein 2 (MECP2) gene with a predominant multisystemic phenotype. The aim of the study is to assess a possible association between MECP2 mutations or RTT disease progression and plasma levels of 4(RS)-4-F4t-Neuroprostane (4-F4t-NeuroP) and 10(RS)-10-F4t-Neuroprostane (10-F4t-NeuroP) in typical RTT patients with proven MECP2 gene mutation. Clinical severity and disease progression were assessed using the Rett clinical severity scale (RCSS) in n = 77 RTT patients. The 4-F4t-NeuroP and 10-F4t-NeuroP molecules were totally synthesized and used to identify the contents of the plasma of the patients. Neuroprostane levels were related to MECP2 mutation category (i.e., early truncating, gene deletion, late truncating, and missense), specific hotspot mutations (i.e., R106W, R133C, R168X, R255X, R270X, R294X, R306C, and T158M), and disease stage (II through IV). Circulating 4-F4t-NeuroP and 10-F4t-NeuroP were significantly related to (i) the type of MECP2 mutations where higher levels were associated to gene deletions (p ≤ 0.001); (ii) severity of common hotspot MECP2 mutation (large deletions, R168X, R255X, and R270X); (iii) disease stage, where higher concentrations were observed at stage II (p ≤ 0.002); and (iv) deficiency in walking (p ≤ 0.0003). This study indicates the biological significance of 4-F4t-NeuroP and 10-F4t-NeuroP as promising molecules to mark the disease progression and potentially gauge genotype-phenotype associations in RTT.
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total synthesis of a docosahexaenoic acid prostanoid using an intramolecular organocatalytic michael reaction of a formyl enal derivative
Organic Letters, 2020Co-Authors: Johanna Revolcavalier, Thierry Durand, Camille Oger, Valerie Bultelponce, Alexandre Guy, Jean-marie GalanoAbstract:The total synthesis of a docosahexaenoic-acid-derived prostaglandin, 4,11-diepi-4-F4t-Neuroprostane, featuring a complex lateral chain was achieved for the first time. A novel prostaglandin cyclope...
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nonenzymatic oxygenated metabolite of docosahexaenoic acid 4 rs 4 f4t Neuroprostane acts as a bioactive lipid molecule in neuronal cells
FEBS Letters, 2020Co-Authors: Jean-marie Galano, Camille Oger, Ho Hang Leung, Laurence Balas, Thierry DurandAbstract:Docosahexaenoic acid (DHA), an abundant fatty acid in the brain, is susceptible to auto-oxidation in situ and releases metabolites such as F4 -Neuroprostane (4-F4t -NeuroP). The presence of 4-F4t -NeuroP in the brain is not well explored. In this study, 4-F4t -NeuroP was introduced into neuroblastoma cells (SH-SY5Y) and, by in vivo infusion, into rodents. Targeted lipidomic analysis of liver and brain tissues shows significant elevation of anti-inflammatory hydroxylated DHA metabolites and an isomer of neuroprotectin D1, suggesting potential beneficial bioactivities of 4-F4t -NeuroP. Additionally, 4-F4t -NeuroP treatment in SH-SY5Y cells and primary neuronal culture consistently upregulates the transcriptional level of the antioxidant enzyme heme oxygenase-1, but the effect is reduced when 4-F4t -NeuroP is further oxidized. Our data suggest that 4-F4t -NeuroP could be neuroprotective in the native state but may have disadvantageous bioactivity when oxidized extensively.
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relevance of 4 f4t Neuroprostane and 10 f4t Neuroprostane to neurological diseases
Free Radical Biology and Medicine, 2018Co-Authors: Cinzia Signorini, Thierry Durand, Camille Oger, Jean-marie Galano, Silvia Leoncini, Lucia Ciccoli, Claudio De Felice, Marisa Carone, Monica Ulivelli, Caterina MannaAbstract:Abstract F4-Neuroprostanes (F4-NeuroPs) are non-enzymatic oxidized products derived from docosahexaenoic acid (DHA) and are suggested to be oxidative damage biomarkers of neurological diseases. However, 128 isomers can be formed from DHA oxidation and among them, 4(RS)−4-F4t-NeuroP (4-F4t-NeuroP) and 10(RS)−10-F4t-NeuroP (10-F4t-NeuroP) are the most studied. Here, we report the identification and the clinical relevance of 4-F4t-NeuroP and 10-F4t-NeuroP in plasma of four different neurological diseases, including multiple sclerosis (MS), autism spectrum disorders (ASD), Rett syndrome (RTT), and Down syndrome (DS). The identification and the optimization of the method were carried out by gas chromatography/negative-ion chemical ionization tandem mass spectrometry (GC/NICI-MS/MS) using chemically synthesized 4-F4t-NeuroP and 10-F4t-NeuroP standards and in oxidized DHA liposome. Both 4-F4t-NeuroP and 10-F4t-NeuroP were detectable in all plasma samples from MS (n = 16), DS (n = 16), ASD (n = 9) and RTT (n = 20) patients. While plasma 10-F4t-NeuroP content was significantly higher in patients of all diseases as compared to age and gender matched healthy control subjects (n = 61), 4-F4t-NeuroP levels were significantly higher in MS and RTT as compared to healthy controls. Significant positive relationships were observed between relative disease severity and 4-F4t-NeuroP levels (r = 0.469, P Overall, by comparing the different types of disease, our plasma data indicates that 4-F4t-NeuroP and 10-F4t -NeuroP: i) are biologically synthesized in vivo and circulated, ii) are related to clinical severity of neurological diseases, iii) are useful to identify shared pathogenetic pathways in distinct brain diseases, and iv) appears to be distinctive for different neurological conditions, thus representing potentially new biological disease markers. Our data strongly suggest that in vivo DHA oxidation follows preferential chemical rearrangements according to different brain diseases.
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Snapshot situation of oxidative degradation of the nervous system, kidney, and adrenal glands biomarkers-Neuroprostane and dihomo-isoprostanes-urinary biomarkers from infancy to elderly adults
Redox Biology, 2017Co-Authors: Libia Alejandra García-flores, Thierry Durand, Camille Oger, Jean-marie Galano, Sonia Medina, Federico Ferreres, Pedro Martínez-hernández, Teresa Casas-pina, Angel Gil-izquierdoAbstract:We analyzed biomarkers of lipid peroxidation of the nervous system -F2-dihomo-isoprostanes, F3-Neuroprostanes, and F4-Neuroprostanes- in urine samples from 158 healthy volunteers ranging from 4 to 88 years old with the aim of analyzing possible associations between their excretion values and age (years). Ten biomarkers were screened in the urine samples by UHPLC-QqQ-MS/MS. Four F2-dihomo-isoprostanes (ent−7-(R)−7-F2t-dihomo-isoprostane, ent−7-epi−7-F2t-dihomo-isoprostane, 17-F2t-dihomo-isoprostane, 17-epi−17-F2t-dihomo-isoprostane), and one DPA-Neuroprostane (4-F3t-Neuroprostane) were detected in the samples. On the one hand, we found a significant, positive correlation (Rho: 0.197, P=0.015) between the age increase and the amount of total F2-dihomo-IsoPs. On the other hand, the values were significantly higher in the childhood group (4–12 years old), when compared to the adolescence group (13–17 years old) and the young adult group (18–35 years old). Surprisingly, no significant differences were found between the middle-aged adults (36–64 years old) and the elderly adults (65–88 years old). We display a snapshot situation of excretory values of oxidative stress biomarkers of the nervous system, using healthy volunteers representative of the different stages of human growth and development. The values reported in this study could be used as a basal or starting point in clinical interventions related to aging processes and/or pathologies associated with the nervous system.
Barry Halliwell - One of the best experts on this subject based on the ideXlab platform.
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oral zinc supplementation does not improve oxidative stress or vascular function in patients with type 2 diabetes with normal zinc levels
Atherosclerosis, 2011Co-Authors: Raymond C S Seet, Amy M L Quek, Huiwen Huang, Shan Hong Huang, Woan Foon Looi, Lee Hua Long, Barry HalliwellAbstract:OBJECTIVE: There is considerable controversy about what constitutes optimal zinc intakes in patients with type 2 diabetes mellitus. Several studies suggest that higher zinc intakes improve vascular function and decrease oxidative damage. We aimed to assess the effects of zinc supplementation using a range of reliable biomarkers of oxidative damage and vascular function in patients with type 2 diabetes. METHODS: Forty male type 2 diabetic patients were supplemented either with 240 mg/day of zinc as zinc gluconate (n=20) or with placebo (n=20) for 3 months. Blood and spot urine samples were taken at baseline, days 3 and 7, months 1, 2 and 3 during supplementation and 1 month after cessation. Serum zinc, reliable biomarkers of oxidative damage (F(2)-isoprostanes, Neuroprostanes, cholesterol oxidation products, allantoin) as well as hydroxyeicosatetraenoic acid products and vascular-related indices (augmentation index, pulse wave velocity and aortic pressure) were measured. RESULTS: Despite significantly higher levels of serum zinc in the treatment group, markers of oxidative damage, levels of hydroxyeicosatetraenoic acid products and vascular indices were unchanged by zinc supplementation during the four-month study period. CONCLUSION: Improving the zinc status in patients with type 2 diabetes with normal zinc levels did not have any impact on oxidative damage and vascular function, and such supplementation may not be generally beneficial in these individuals.
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oral zinc supplementation does not improve oxidative stress or vascular function in patients with type 2 diabetes with normal zinc levels
Atherosclerosis, 2011Co-Authors: Raymond C S Seet, Amy M L Quek, Huiwen Huang, Shan Hong Huang, Woan Foon Looi, Lee Hua Long, Chungyung J Lee, Erle C H Lim, Barry HalliwellAbstract:Objective: There is considerable controversy about what constitutes optimal zinc intakes in patients with type 2 diabetes mellitus. Several studies suggest that higher zinc intakes improve vascular function and decrease oxidative damage. We aimed to assess the effects of zinc supplementation using a range of reliable biomarkers of oxidative damage and vascular function in patients with type 2 diabetes. Methods: Forty male type 2 diabetic patients were supplemented either with 240 mg/day of zinc as zinc gluconate (n = 20) or with placebo (n = 20) for 3 months. Blood and spot urine samples were taken at baseline, days 3 and 7, months 1, 2 and 3 during supplementation and 1 month after cessation. Serum zinc, reliable biomarkers of oxidative damage (F2-isoprostanes, Neuroprostanes, cholesterol oxidation products, allantoin) as well as hydroxyeicosatetraenoic acid products and vascular-related indices (augmentation index, pulse wave velocity and aortic pressure) were measured. Results: Despite significantly higher levels of serum zinc in the treatment group, markers of oxidative damage, levels of hydroxyeicosatetraenoic acid products and vascular indices were unchanged by zinc supplementation during the four-month study period. Conclusion: Improving the zinc status in patients with type 2 diabetes with normal zinc levels did not have any impact on oxidative damage and vascular function, and such supplementation may not be generally beneficial in these individuals. © 2011 Elsevier Ireland Ltd. All rights reserved.
Raymond C S Seet - One of the best experts on this subject based on the ideXlab platform.
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oral zinc supplementation does not improve oxidative stress or vascular function in patients with type 2 diabetes with normal zinc levels
Atherosclerosis, 2011Co-Authors: Raymond C S Seet, Amy M L Quek, Huiwen Huang, Shan Hong Huang, Woan Foon Looi, Lee Hua Long, Barry HalliwellAbstract:OBJECTIVE: There is considerable controversy about what constitutes optimal zinc intakes in patients with type 2 diabetes mellitus. Several studies suggest that higher zinc intakes improve vascular function and decrease oxidative damage. We aimed to assess the effects of zinc supplementation using a range of reliable biomarkers of oxidative damage and vascular function in patients with type 2 diabetes. METHODS: Forty male type 2 diabetic patients were supplemented either with 240 mg/day of zinc as zinc gluconate (n=20) or with placebo (n=20) for 3 months. Blood and spot urine samples were taken at baseline, days 3 and 7, months 1, 2 and 3 during supplementation and 1 month after cessation. Serum zinc, reliable biomarkers of oxidative damage (F(2)-isoprostanes, Neuroprostanes, cholesterol oxidation products, allantoin) as well as hydroxyeicosatetraenoic acid products and vascular-related indices (augmentation index, pulse wave velocity and aortic pressure) were measured. RESULTS: Despite significantly higher levels of serum zinc in the treatment group, markers of oxidative damage, levels of hydroxyeicosatetraenoic acid products and vascular indices were unchanged by zinc supplementation during the four-month study period. CONCLUSION: Improving the zinc status in patients with type 2 diabetes with normal zinc levels did not have any impact on oxidative damage and vascular function, and such supplementation may not be generally beneficial in these individuals.
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oral zinc supplementation does not improve oxidative stress or vascular function in patients with type 2 diabetes with normal zinc levels
Atherosclerosis, 2011Co-Authors: Raymond C S Seet, Amy M L Quek, Huiwen Huang, Shan Hong Huang, Woan Foon Looi, Lee Hua Long, Chungyung J Lee, Erle C H Lim, Barry HalliwellAbstract:Objective: There is considerable controversy about what constitutes optimal zinc intakes in patients with type 2 diabetes mellitus. Several studies suggest that higher zinc intakes improve vascular function and decrease oxidative damage. We aimed to assess the effects of zinc supplementation using a range of reliable biomarkers of oxidative damage and vascular function in patients with type 2 diabetes. Methods: Forty male type 2 diabetic patients were supplemented either with 240 mg/day of zinc as zinc gluconate (n = 20) or with placebo (n = 20) for 3 months. Blood and spot urine samples were taken at baseline, days 3 and 7, months 1, 2 and 3 during supplementation and 1 month after cessation. Serum zinc, reliable biomarkers of oxidative damage (F2-isoprostanes, Neuroprostanes, cholesterol oxidation products, allantoin) as well as hydroxyeicosatetraenoic acid products and vascular-related indices (augmentation index, pulse wave velocity and aortic pressure) were measured. Results: Despite significantly higher levels of serum zinc in the treatment group, markers of oxidative damage, levels of hydroxyeicosatetraenoic acid products and vascular indices were unchanged by zinc supplementation during the four-month study period. Conclusion: Improving the zinc status in patients with type 2 diabetes with normal zinc levels did not have any impact on oxidative damage and vascular function, and such supplementation may not be generally beneficial in these individuals. © 2011 Elsevier Ireland Ltd. All rights reserved.