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Ahng Kong - One of the best experts on this subject based on the ideXlab platform.
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Induction of Heme Oxygenase-1 (HO-1) and NAD[P]H: Quinone Oxidoreductase 1 (NQO1) by a Phenolic Antioxidant, Butylated Hydroxyanisole (BHA) and Its Metabolite, tert-Butylhydroquinone (tBHQ) in Primary-Cultured Human and Rat Hepatocytes
Pharmaceutical Research, 2006Co-Authors: Youngsam Keum, Celine Liew, Xiaoling Yuan, Michael P Shakarjian, Saeho Chong, Yong-hae Han, Jung-hwan Kim, Ahng KongAbstract:Purpose This study was aimed to investigate the effects of a Phenolic Antioxidant, butylated hydroxyanisole (BHA) and its metabolite, tert -butylhydroquinone (tBHQ) on the induction of HO-1, NQO1 and Nrf2 proteins and their regulatory mechanisms in primary-cultured hepatocytes. Methods After exposure of BHA and tBHQ to primary-cultured rat and human hepatocytes and mouse neonatal fibroblasts (MFs), Western blot, semi-quantitative RT-PCR and microarray analysis were conducted. Results Induction of HO-1, NQO1 and Nrf2 proteins and activation of ERK1/2 and JNK1/2 were observed after BHA and tBHQ treatments in primary-cultured rat and human hepatocytes. Semi-quantitative RT-PCR study and microarray analysis revealed that HO-1 and NQO1 were transcriptionally activated in primary-cultured rat hepatocytes and a substantial transcriptional activation, including HO-1 occurred in primary-cultured human hepatocytes after BHA treatment. Whereas BHA failed to induce HO-1 in wild-type and Nrf2 knock-out MFs, tBHQ strongly induced HO-1 in wild-type, but not in Nrf2 knock-out MFs. Conclusions Our data demonstrate that both BHA and tBHQ are strong chemical inducers of HO-1, NQO1 and Nrf2 proteins in primary-cultured human and rat hepatocytes with the activation of MAPK ERK1/2 and JNK1/2. However, in MFs, BHA failed to induce HO-1, whereas tBHQ strongly induced HO-1 in Nrf2 wild-type but not in Nrf2 knock-out, suggesting that Nrf2 is indispensable for tBHQ-induced HO-1 in MF.
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induction of heme oxygenase 1 ho 1 and nad p h quinone oxidoreductase 1 nqo1 by a Phenolic Antioxidant butylated hydroxyanisole bha and its metabolite tert butylhydroquinone tbhq in primary cultured human and rat hepatocytes
Pharmaceutical Research, 2006Co-Authors: Youngsam Keum, Celine Liew, Changjiang Xu, Xiaoling Yuan, Michael P Shakarjian, Saeho Chong, Ahng KongAbstract:This study was aimed to investigate the effects of a Phenolic Antioxidant, butylated hydroxyanisole (BHA) and its metabolite, tert-butylhydroquinone (tBHQ) on the induction of HO-1, NQO1 and Nrf2 proteins and their regulatory mechanisms in primary-cultured hepatocytes. After exposure of BHA and tBHQ to primary-cultured rat and human hepatocytes and mouse neonatal fibroblasts (MFs), Western blot, semi-quantitative RT-PCR and microarray analysis were conducted. Induction of HO-1, NQO1 and Nrf2 proteins and activation of ERK1/2 and JNK1/2 were observed after BHA and tBHQ treatments in primary-cultured rat and human hepatocytes. Semi-quantitative RT-PCR study and microarray analysis revealed that HO-1 and NQO1 were transcriptionally activated in primary-cultured rat hepatocytes and a substantial transcriptional activation, including HO-1 occurred in primary-cultured human hepatocytes after BHA treatment. Whereas BHA failed to induce HO-1 in wild-type and Nrf2 knock-out MFs, tBHQ strongly induced HO-1 in wild-type, but not in Nrf2 knock-out MFs. Our data demonstrate that both BHA and tBHQ are strong chemical inducers of HO-1, NQO1 and Nrf2 proteins in primary-cultured human and rat hepatocytes with the activation of MAPK ERK1/2 and JNK1/2. However, in MFs, BHA failed to induce HO-1, whereas tBHQ strongly induced HO-1 in Nrf2 wild-type but not in Nrf2 knock-out, suggesting that Nrf2 is indispensable for tBHQ-induced HO-1 in MF.
Jean-luc Gardette - One of the best experts on this subject based on the ideXlab platform.
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Photochemical behaviour of fire-retarded polymers
Polymer Degradation and Stability, 2010Co-Authors: D. Chantegraille, Sandrine Morlat-therias, Jean-luc GardetteAbstract:The influence of a non-halogenated intumescent fire retardant on the photooxidation of polypropylene is reported. The photooxidation of polypropylene stabilised with a Phenolic Antioxidant and two redox Antioxidants (HALS), without and with the flame retardant has been studied. The chemical modifications resulting from UV-light exposure with wavelengths above 300 nm in the presence of oxygen were followed by IR and UV-visible spectroscopies. Special attention was given to the influence of each component on the rate of oxidation of the polymeric matrix. The photooxidation of the fire-retarded polymer can be described by two independent phenomena: the photooxidation of the intumescent agent and the photooxidation of the polymer. The results obtained offer new insight in the formulation of stabilised fire-retarded PP for outdoors applications.
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photooxidation of polypropylene montmorillonite nanocomposites 2 interactions with Antioxidants
Chemistry of Materials, 2005Co-Authors: Sandrine Morlattherias, Bénédicte Mailhot, And David Gonzalez, Jean-luc GardetteAbstract:The influence of stabilizing additives on the photooxidation of polypropylene/montmorillonite (PP/MMt) nanocomposites exposed to UV light was studied. Two different stabilizers were used, a Phenolic Antioxidant and a redox Antioxidant. A significant reduction in the induction period of oxidation was observed in the presence of MMt. This is believed to arise from interactions between the additives and the nanoclay. The interactions could involve the adsorption of additives onto the clay, the degradation of the alkylammonium cations exchanged in MMt, and the catalytic effect of iron impurities of the organomontmorillonite. Iron could catalyze the decomposition of the primary hydroperoxides formed by photooxidation of PP, which would in turn accelerate the additive consumption and decrease the length of the period before the permanent regime of oxidation is reached.
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Photooxidation of Polypropylene/Montmorillonite Nanocomposites. 2. Interactions with Antioxidants.
Chemistry of Materials, 2005Co-Authors: Jean-luc Gardette, Sandrine Morlat-therias, Bénédicte Mailhot, David GonzalezAbstract:The influence of stabilizing additives on the photooxidation of polypropylene/montmorillonite (PP/ MMt) nanocomposites exposed to UV light was studied. Two différent stabilizers were used, a Phenolic Antioxidant and a redox Antioxidant. A significant reduction in the induction period of oxidation was observed in the presence of MMt. This is believed to arise from interactions between the additives and the nanoclay. The interactions could involve the adsorption of additives onto the clay, the degradation of the alkylammonium cations exchanged in MMt, and the catalytic effect of iron impurities of the organomontmorillonite. Iron could catalyze the decomposition of the primary hydroperoxides formed by photooxidation of PP, which would in turn accelerate the additive consumption and decrease the length of the period before the permanent regime of oxidation is reached.
Youngsam Keum - One of the best experts on this subject based on the ideXlab platform.
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Induction of Heme Oxygenase-1 (HO-1) and NAD[P]H: Quinone Oxidoreductase 1 (NQO1) by a Phenolic Antioxidant, Butylated Hydroxyanisole (BHA) and Its Metabolite, tert-Butylhydroquinone (tBHQ) in Primary-Cultured Human and Rat Hepatocytes
Pharmaceutical Research, 2006Co-Authors: Youngsam Keum, Celine Liew, Xiaoling Yuan, Michael P Shakarjian, Saeho Chong, Yong-hae Han, Jung-hwan Kim, Ahng KongAbstract:Purpose This study was aimed to investigate the effects of a Phenolic Antioxidant, butylated hydroxyanisole (BHA) and its metabolite, tert -butylhydroquinone (tBHQ) on the induction of HO-1, NQO1 and Nrf2 proteins and their regulatory mechanisms in primary-cultured hepatocytes. Methods After exposure of BHA and tBHQ to primary-cultured rat and human hepatocytes and mouse neonatal fibroblasts (MFs), Western blot, semi-quantitative RT-PCR and microarray analysis were conducted. Results Induction of HO-1, NQO1 and Nrf2 proteins and activation of ERK1/2 and JNK1/2 were observed after BHA and tBHQ treatments in primary-cultured rat and human hepatocytes. Semi-quantitative RT-PCR study and microarray analysis revealed that HO-1 and NQO1 were transcriptionally activated in primary-cultured rat hepatocytes and a substantial transcriptional activation, including HO-1 occurred in primary-cultured human hepatocytes after BHA treatment. Whereas BHA failed to induce HO-1 in wild-type and Nrf2 knock-out MFs, tBHQ strongly induced HO-1 in wild-type, but not in Nrf2 knock-out MFs. Conclusions Our data demonstrate that both BHA and tBHQ are strong chemical inducers of HO-1, NQO1 and Nrf2 proteins in primary-cultured human and rat hepatocytes with the activation of MAPK ERK1/2 and JNK1/2. However, in MFs, BHA failed to induce HO-1, whereas tBHQ strongly induced HO-1 in Nrf2 wild-type but not in Nrf2 knock-out, suggesting that Nrf2 is indispensable for tBHQ-induced HO-1 in MF.
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induction of heme oxygenase 1 ho 1 and nad p h quinone oxidoreductase 1 nqo1 by a Phenolic Antioxidant butylated hydroxyanisole bha and its metabolite tert butylhydroquinone tbhq in primary cultured human and rat hepatocytes
Pharmaceutical Research, 2006Co-Authors: Youngsam Keum, Celine Liew, Changjiang Xu, Xiaoling Yuan, Michael P Shakarjian, Saeho Chong, Ahng KongAbstract:This study was aimed to investigate the effects of a Phenolic Antioxidant, butylated hydroxyanisole (BHA) and its metabolite, tert-butylhydroquinone (tBHQ) on the induction of HO-1, NQO1 and Nrf2 proteins and their regulatory mechanisms in primary-cultured hepatocytes. After exposure of BHA and tBHQ to primary-cultured rat and human hepatocytes and mouse neonatal fibroblasts (MFs), Western blot, semi-quantitative RT-PCR and microarray analysis were conducted. Induction of HO-1, NQO1 and Nrf2 proteins and activation of ERK1/2 and JNK1/2 were observed after BHA and tBHQ treatments in primary-cultured rat and human hepatocytes. Semi-quantitative RT-PCR study and microarray analysis revealed that HO-1 and NQO1 were transcriptionally activated in primary-cultured rat hepatocytes and a substantial transcriptional activation, including HO-1 occurred in primary-cultured human hepatocytes after BHA treatment. Whereas BHA failed to induce HO-1 in wild-type and Nrf2 knock-out MFs, tBHQ strongly induced HO-1 in wild-type, but not in Nrf2 knock-out MFs. Our data demonstrate that both BHA and tBHQ are strong chemical inducers of HO-1, NQO1 and Nrf2 proteins in primary-cultured human and rat hepatocytes with the activation of MAPK ERK1/2 and JNK1/2. However, in MFs, BHA failed to induce HO-1, whereas tBHQ strongly induced HO-1 in Nrf2 wild-type but not in Nrf2 knock-out, suggesting that Nrf2 is indispensable for tBHQ-induced HO-1 in MF.
Celine Liew - One of the best experts on this subject based on the ideXlab platform.
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Induction of Heme Oxygenase-1 (HO-1) and NAD[P]H: Quinone Oxidoreductase 1 (NQO1) by a Phenolic Antioxidant, Butylated Hydroxyanisole (BHA) and Its Metabolite, tert-Butylhydroquinone (tBHQ) in Primary-Cultured Human and Rat Hepatocytes
Pharmaceutical Research, 2006Co-Authors: Youngsam Keum, Celine Liew, Xiaoling Yuan, Michael P Shakarjian, Saeho Chong, Yong-hae Han, Jung-hwan Kim, Ahng KongAbstract:Purpose This study was aimed to investigate the effects of a Phenolic Antioxidant, butylated hydroxyanisole (BHA) and its metabolite, tert -butylhydroquinone (tBHQ) on the induction of HO-1, NQO1 and Nrf2 proteins and their regulatory mechanisms in primary-cultured hepatocytes. Methods After exposure of BHA and tBHQ to primary-cultured rat and human hepatocytes and mouse neonatal fibroblasts (MFs), Western blot, semi-quantitative RT-PCR and microarray analysis were conducted. Results Induction of HO-1, NQO1 and Nrf2 proteins and activation of ERK1/2 and JNK1/2 were observed after BHA and tBHQ treatments in primary-cultured rat and human hepatocytes. Semi-quantitative RT-PCR study and microarray analysis revealed that HO-1 and NQO1 were transcriptionally activated in primary-cultured rat hepatocytes and a substantial transcriptional activation, including HO-1 occurred in primary-cultured human hepatocytes after BHA treatment. Whereas BHA failed to induce HO-1 in wild-type and Nrf2 knock-out MFs, tBHQ strongly induced HO-1 in wild-type, but not in Nrf2 knock-out MFs. Conclusions Our data demonstrate that both BHA and tBHQ are strong chemical inducers of HO-1, NQO1 and Nrf2 proteins in primary-cultured human and rat hepatocytes with the activation of MAPK ERK1/2 and JNK1/2. However, in MFs, BHA failed to induce HO-1, whereas tBHQ strongly induced HO-1 in Nrf2 wild-type but not in Nrf2 knock-out, suggesting that Nrf2 is indispensable for tBHQ-induced HO-1 in MF.
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induction of heme oxygenase 1 ho 1 and nad p h quinone oxidoreductase 1 nqo1 by a Phenolic Antioxidant butylated hydroxyanisole bha and its metabolite tert butylhydroquinone tbhq in primary cultured human and rat hepatocytes
Pharmaceutical Research, 2006Co-Authors: Youngsam Keum, Celine Liew, Changjiang Xu, Xiaoling Yuan, Michael P Shakarjian, Saeho Chong, Ahng KongAbstract:This study was aimed to investigate the effects of a Phenolic Antioxidant, butylated hydroxyanisole (BHA) and its metabolite, tert-butylhydroquinone (tBHQ) on the induction of HO-1, NQO1 and Nrf2 proteins and their regulatory mechanisms in primary-cultured hepatocytes. After exposure of BHA and tBHQ to primary-cultured rat and human hepatocytes and mouse neonatal fibroblasts (MFs), Western blot, semi-quantitative RT-PCR and microarray analysis were conducted. Induction of HO-1, NQO1 and Nrf2 proteins and activation of ERK1/2 and JNK1/2 were observed after BHA and tBHQ treatments in primary-cultured rat and human hepatocytes. Semi-quantitative RT-PCR study and microarray analysis revealed that HO-1 and NQO1 were transcriptionally activated in primary-cultured rat hepatocytes and a substantial transcriptional activation, including HO-1 occurred in primary-cultured human hepatocytes after BHA treatment. Whereas BHA failed to induce HO-1 in wild-type and Nrf2 knock-out MFs, tBHQ strongly induced HO-1 in wild-type, but not in Nrf2 knock-out MFs. Our data demonstrate that both BHA and tBHQ are strong chemical inducers of HO-1, NQO1 and Nrf2 proteins in primary-cultured human and rat hepatocytes with the activation of MAPK ERK1/2 and JNK1/2. However, in MFs, BHA failed to induce HO-1, whereas tBHQ strongly induced HO-1 in Nrf2 wild-type but not in Nrf2 knock-out, suggesting that Nrf2 is indispensable for tBHQ-induced HO-1 in MF.
Xiaoling Yuan - One of the best experts on this subject based on the ideXlab platform.
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Induction of Heme Oxygenase-1 (HO-1) and NAD[P]H: Quinone Oxidoreductase 1 (NQO1) by a Phenolic Antioxidant, Butylated Hydroxyanisole (BHA) and Its Metabolite, tert-Butylhydroquinone (tBHQ) in Primary-Cultured Human and Rat Hepatocytes
Pharmaceutical Research, 2006Co-Authors: Youngsam Keum, Celine Liew, Xiaoling Yuan, Michael P Shakarjian, Saeho Chong, Yong-hae Han, Jung-hwan Kim, Ahng KongAbstract:Purpose This study was aimed to investigate the effects of a Phenolic Antioxidant, butylated hydroxyanisole (BHA) and its metabolite, tert -butylhydroquinone (tBHQ) on the induction of HO-1, NQO1 and Nrf2 proteins and their regulatory mechanisms in primary-cultured hepatocytes. Methods After exposure of BHA and tBHQ to primary-cultured rat and human hepatocytes and mouse neonatal fibroblasts (MFs), Western blot, semi-quantitative RT-PCR and microarray analysis were conducted. Results Induction of HO-1, NQO1 and Nrf2 proteins and activation of ERK1/2 and JNK1/2 were observed after BHA and tBHQ treatments in primary-cultured rat and human hepatocytes. Semi-quantitative RT-PCR study and microarray analysis revealed that HO-1 and NQO1 were transcriptionally activated in primary-cultured rat hepatocytes and a substantial transcriptional activation, including HO-1 occurred in primary-cultured human hepatocytes after BHA treatment. Whereas BHA failed to induce HO-1 in wild-type and Nrf2 knock-out MFs, tBHQ strongly induced HO-1 in wild-type, but not in Nrf2 knock-out MFs. Conclusions Our data demonstrate that both BHA and tBHQ are strong chemical inducers of HO-1, NQO1 and Nrf2 proteins in primary-cultured human and rat hepatocytes with the activation of MAPK ERK1/2 and JNK1/2. However, in MFs, BHA failed to induce HO-1, whereas tBHQ strongly induced HO-1 in Nrf2 wild-type but not in Nrf2 knock-out, suggesting that Nrf2 is indispensable for tBHQ-induced HO-1 in MF.
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induction of heme oxygenase 1 ho 1 and nad p h quinone oxidoreductase 1 nqo1 by a Phenolic Antioxidant butylated hydroxyanisole bha and its metabolite tert butylhydroquinone tbhq in primary cultured human and rat hepatocytes
Pharmaceutical Research, 2006Co-Authors: Youngsam Keum, Celine Liew, Changjiang Xu, Xiaoling Yuan, Michael P Shakarjian, Saeho Chong, Ahng KongAbstract:This study was aimed to investigate the effects of a Phenolic Antioxidant, butylated hydroxyanisole (BHA) and its metabolite, tert-butylhydroquinone (tBHQ) on the induction of HO-1, NQO1 and Nrf2 proteins and their regulatory mechanisms in primary-cultured hepatocytes. After exposure of BHA and tBHQ to primary-cultured rat and human hepatocytes and mouse neonatal fibroblasts (MFs), Western blot, semi-quantitative RT-PCR and microarray analysis were conducted. Induction of HO-1, NQO1 and Nrf2 proteins and activation of ERK1/2 and JNK1/2 were observed after BHA and tBHQ treatments in primary-cultured rat and human hepatocytes. Semi-quantitative RT-PCR study and microarray analysis revealed that HO-1 and NQO1 were transcriptionally activated in primary-cultured rat hepatocytes and a substantial transcriptional activation, including HO-1 occurred in primary-cultured human hepatocytes after BHA treatment. Whereas BHA failed to induce HO-1 in wild-type and Nrf2 knock-out MFs, tBHQ strongly induced HO-1 in wild-type, but not in Nrf2 knock-out MFs. Our data demonstrate that both BHA and tBHQ are strong chemical inducers of HO-1, NQO1 and Nrf2 proteins in primary-cultured human and rat hepatocytes with the activation of MAPK ERK1/2 and JNK1/2. However, in MFs, BHA failed to induce HO-1, whereas tBHQ strongly induced HO-1 in Nrf2 wild-type but not in Nrf2 knock-out, suggesting that Nrf2 is indispensable for tBHQ-induced HO-1 in MF.