The Experts below are selected from a list of 1614 Experts worldwide ranked by ideXlab platform
Taro Shuin - One of the best experts on this subject based on the ideXlab platform.
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mechanism of cell death by 5 aminolevulinic acid based photodynamic action and its enhancement by ferrochelatase inhibitors in human Histiocytic Lymphoma cell line u937
Cell Biochemistry and Function, 2009Co-Authors: Takashi Amo, Keiji Inoue, Hirofumi Fujita, Noriaki Kawanishi, Masataka Uchida, Eri Oyanagi, Toshihiko Utsumi, Tetsuya Ogino, Taro ShuinAbstract:Photodynamic therapy (PDT) for tumors is based on the tumor-selective accumulation of a photosensitizer, protoporphyrin IX (PpIX), followed by irradiation with visible light. However, the molecular mechanism of cell death caused by PDT has not been fully elucidated. The 5-aminolevulinic acid (ALA)-based photodynamic action (PDA) was dependent on the accumulation of PpIX, the level of which decreased rapidly by eliminating ALA from the incubation medium in human Histiocytic Lymphoma U937 cells. PDA induced apoptosis characterized by lipid peroxidation, increase in Bak and Bax/Bcl-xL, decrease in Bid, membrane depolarization, cytochrome c release, caspase-3 activation, phosphatidylserine (PS) externalization. PDT-induced cell death seemed to occur predominantly via apoptosis through distribution of PpIX in mitochondria. These cell death events were enhanced by ferrochelatase inhibitors. These results indicated that ALA-based-PDA induced apoptotic cell death through a mitochondrial pathway and that ferrochelatase inhibitors might enhanced the effect of PDT for tumors even at low concentrations of ALA. Copyright © 2009 John Wiley & Sons, Ltd.
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mechanism of cell death by 5 aminolevulinic acid based photodynamic action and its enhancement by ferrochelatase inhibitors in human Histiocytic Lymphoma cell line u937
Cell Biochemistry and Function, 2009Co-Authors: Takashi Amo, Keiji Inoue, Hirofumi Fujita, Noriaki Kawanishi, Masataka Uchida, Eri Oyanagi, Toshihiko Utsumi, Tetsuya Ogino, Taro ShuinAbstract:Photodynamic therapy (PDT) for tumors is based on the tumor-selective accumulation of a photosensitizer, protoporphyrin IX (PpIX), followed by irradiation with visible light. However, the molecular mechanism of cell death caused by PDT has not been fully elucidated. The 5-aminolevulinic acid (ALA)-based photodynamic action (PDA) was dependent on the accumulation of PpIX, the level of which decreased rapidly by eliminating ALA from the incubation medium in human Histiocytic Lymphoma U937 cells. PDA induced apoptosis characterized by lipid peroxidation, increase in Bak and Bax/Bcl-xL, decrease in Bid, membrane depolarization, cytochrome c release, caspase-3 activation, phosphatidylserine (PS) externalization. PDT-induced cell death seemed to occur predominantly via apoptosis through distribution of PpIX in mitochondria. These cell death events were enhanced by ferrochelatase inhibitors. These results indicated that ALA-based-PDA induced apoptotic cell death through a mitochondrial pathway and that ferrochelatase inhibitors might enhanced the effect of PDT for tumors even at low concentrations of ALA.
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regulation of 5 aminolevulinic acid dependent protoporphyrin ix accumulations in human Histiocytic Lymphoma u937 cells
Physiological chemistry and physics and medical NMR, 2007Co-Authors: Yuya Okimura, Keiji Inoue, Hirofumi Fujita, Taro Shuin, Tetsuya Ogino, Hiromi Yano, Tatsuji Yasuda, Masayasu Inoue, Kozo Utsumi, Junzo SasakiAbstract:The aim of the present work is to clarify the mechanism(s) that regulates the accumulation of protoporphyrin IX (PpIX) in human Histiocytic Lymphoma cell line U937 incubated with 5-aminolevulinic acid (ALA). Biosynthesis and accumulation of PpIX in the cells was determined after incubation with 0.1-5 mM ALA using a flow cytometric technique. The synthesized endogenous PpIX was found to localize predominantly in the mitochondrial region of the cells. The ALA-enhanced PpIX synthesis was suppressed by the presence of either beta-alanine, a competitive inhibitor of beta-transporters on cell membranes, or carbonyl cyanide p-trifluoromethoxyphenyl hydrazone, an uncoupler of mitochondrial oxidative phosphorylation. In contrast, cellular accumulation of PpIX was enhanced by the presence of either deferoxamine (an iron chelater), MnCl2 (a ferrochelatase inhibitor), or Sn-mesoporphyrin (heme oxygenase inhibitor). These results suggest that ALA-enhanced accumulation of PpIX in U937 cells was regulated by cellular uptake and conversion of ALA to PpIX and by degradation of Heme.
Noriaki Kawanishi - One of the best experts on this subject based on the ideXlab platform.
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mechanism of cell death by 5 aminolevulinic acid based photodynamic action and its enhancement by ferrochelatase inhibitors in human Histiocytic Lymphoma cell line u937
Cell Biochemistry and Function, 2009Co-Authors: Takashi Amo, Keiji Inoue, Hirofumi Fujita, Noriaki Kawanishi, Masataka Uchida, Eri Oyanagi, Toshihiko Utsumi, Tetsuya Ogino, Taro ShuinAbstract:Photodynamic therapy (PDT) for tumors is based on the tumor-selective accumulation of a photosensitizer, protoporphyrin IX (PpIX), followed by irradiation with visible light. However, the molecular mechanism of cell death caused by PDT has not been fully elucidated. The 5-aminolevulinic acid (ALA)-based photodynamic action (PDA) was dependent on the accumulation of PpIX, the level of which decreased rapidly by eliminating ALA from the incubation medium in human Histiocytic Lymphoma U937 cells. PDA induced apoptosis characterized by lipid peroxidation, increase in Bak and Bax/Bcl-xL, decrease in Bid, membrane depolarization, cytochrome c release, caspase-3 activation, phosphatidylserine (PS) externalization. PDT-induced cell death seemed to occur predominantly via apoptosis through distribution of PpIX in mitochondria. These cell death events were enhanced by ferrochelatase inhibitors. These results indicated that ALA-based-PDA induced apoptotic cell death through a mitochondrial pathway and that ferrochelatase inhibitors might enhanced the effect of PDT for tumors even at low concentrations of ALA. Copyright © 2009 John Wiley & Sons, Ltd.
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mechanism of cell death by 5 aminolevulinic acid based photodynamic action and its enhancement by ferrochelatase inhibitors in human Histiocytic Lymphoma cell line u937
Cell Biochemistry and Function, 2009Co-Authors: Takashi Amo, Keiji Inoue, Hirofumi Fujita, Noriaki Kawanishi, Masataka Uchida, Eri Oyanagi, Toshihiko Utsumi, Tetsuya Ogino, Taro ShuinAbstract:Photodynamic therapy (PDT) for tumors is based on the tumor-selective accumulation of a photosensitizer, protoporphyrin IX (PpIX), followed by irradiation with visible light. However, the molecular mechanism of cell death caused by PDT has not been fully elucidated. The 5-aminolevulinic acid (ALA)-based photodynamic action (PDA) was dependent on the accumulation of PpIX, the level of which decreased rapidly by eliminating ALA from the incubation medium in human Histiocytic Lymphoma U937 cells. PDA induced apoptosis characterized by lipid peroxidation, increase in Bak and Bax/Bcl-xL, decrease in Bid, membrane depolarization, cytochrome c release, caspase-3 activation, phosphatidylserine (PS) externalization. PDT-induced cell death seemed to occur predominantly via apoptosis through distribution of PpIX in mitochondria. These cell death events were enhanced by ferrochelatase inhibitors. These results indicated that ALA-based-PDA induced apoptotic cell death through a mitochondrial pathway and that ferrochelatase inhibitors might enhanced the effect of PDT for tumors even at low concentrations of ALA.
Takashi Amo - One of the best experts on this subject based on the ideXlab platform.
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mechanism of cell death by 5 aminolevulinic acid based photodynamic action and its enhancement by ferrochelatase inhibitors in human Histiocytic Lymphoma cell line u937
Cell Biochemistry and Function, 2009Co-Authors: Takashi Amo, Keiji Inoue, Hirofumi Fujita, Noriaki Kawanishi, Masataka Uchida, Eri Oyanagi, Toshihiko Utsumi, Tetsuya Ogino, Taro ShuinAbstract:Photodynamic therapy (PDT) for tumors is based on the tumor-selective accumulation of a photosensitizer, protoporphyrin IX (PpIX), followed by irradiation with visible light. However, the molecular mechanism of cell death caused by PDT has not been fully elucidated. The 5-aminolevulinic acid (ALA)-based photodynamic action (PDA) was dependent on the accumulation of PpIX, the level of which decreased rapidly by eliminating ALA from the incubation medium in human Histiocytic Lymphoma U937 cells. PDA induced apoptosis characterized by lipid peroxidation, increase in Bak and Bax/Bcl-xL, decrease in Bid, membrane depolarization, cytochrome c release, caspase-3 activation, phosphatidylserine (PS) externalization. PDT-induced cell death seemed to occur predominantly via apoptosis through distribution of PpIX in mitochondria. These cell death events were enhanced by ferrochelatase inhibitors. These results indicated that ALA-based-PDA induced apoptotic cell death through a mitochondrial pathway and that ferrochelatase inhibitors might enhanced the effect of PDT for tumors even at low concentrations of ALA. Copyright © 2009 John Wiley & Sons, Ltd.
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mechanism of cell death by 5 aminolevulinic acid based photodynamic action and its enhancement by ferrochelatase inhibitors in human Histiocytic Lymphoma cell line u937
Cell Biochemistry and Function, 2009Co-Authors: Takashi Amo, Keiji Inoue, Hirofumi Fujita, Noriaki Kawanishi, Masataka Uchida, Eri Oyanagi, Toshihiko Utsumi, Tetsuya Ogino, Taro ShuinAbstract:Photodynamic therapy (PDT) for tumors is based on the tumor-selective accumulation of a photosensitizer, protoporphyrin IX (PpIX), followed by irradiation with visible light. However, the molecular mechanism of cell death caused by PDT has not been fully elucidated. The 5-aminolevulinic acid (ALA)-based photodynamic action (PDA) was dependent on the accumulation of PpIX, the level of which decreased rapidly by eliminating ALA from the incubation medium in human Histiocytic Lymphoma U937 cells. PDA induced apoptosis characterized by lipid peroxidation, increase in Bak and Bax/Bcl-xL, decrease in Bid, membrane depolarization, cytochrome c release, caspase-3 activation, phosphatidylserine (PS) externalization. PDT-induced cell death seemed to occur predominantly via apoptosis through distribution of PpIX in mitochondria. These cell death events were enhanced by ferrochelatase inhibitors. These results indicated that ALA-based-PDA induced apoptotic cell death through a mitochondrial pathway and that ferrochelatase inhibitors might enhanced the effect of PDT for tumors even at low concentrations of ALA.
Tetsuya Ogino - One of the best experts on this subject based on the ideXlab platform.
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mechanism of cell death by 5 aminolevulinic acid based photodynamic action and its enhancement by ferrochelatase inhibitors in human Histiocytic Lymphoma cell line u937
Cell Biochemistry and Function, 2009Co-Authors: Takashi Amo, Keiji Inoue, Hirofumi Fujita, Noriaki Kawanishi, Masataka Uchida, Eri Oyanagi, Toshihiko Utsumi, Tetsuya Ogino, Taro ShuinAbstract:Photodynamic therapy (PDT) for tumors is based on the tumor-selective accumulation of a photosensitizer, protoporphyrin IX (PpIX), followed by irradiation with visible light. However, the molecular mechanism of cell death caused by PDT has not been fully elucidated. The 5-aminolevulinic acid (ALA)-based photodynamic action (PDA) was dependent on the accumulation of PpIX, the level of which decreased rapidly by eliminating ALA from the incubation medium in human Histiocytic Lymphoma U937 cells. PDA induced apoptosis characterized by lipid peroxidation, increase in Bak and Bax/Bcl-xL, decrease in Bid, membrane depolarization, cytochrome c release, caspase-3 activation, phosphatidylserine (PS) externalization. PDT-induced cell death seemed to occur predominantly via apoptosis through distribution of PpIX in mitochondria. These cell death events were enhanced by ferrochelatase inhibitors. These results indicated that ALA-based-PDA induced apoptotic cell death through a mitochondrial pathway and that ferrochelatase inhibitors might enhanced the effect of PDT for tumors even at low concentrations of ALA. Copyright © 2009 John Wiley & Sons, Ltd.
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mechanism of cell death by 5 aminolevulinic acid based photodynamic action and its enhancement by ferrochelatase inhibitors in human Histiocytic Lymphoma cell line u937
Cell Biochemistry and Function, 2009Co-Authors: Takashi Amo, Keiji Inoue, Hirofumi Fujita, Noriaki Kawanishi, Masataka Uchida, Eri Oyanagi, Toshihiko Utsumi, Tetsuya Ogino, Taro ShuinAbstract:Photodynamic therapy (PDT) for tumors is based on the tumor-selective accumulation of a photosensitizer, protoporphyrin IX (PpIX), followed by irradiation with visible light. However, the molecular mechanism of cell death caused by PDT has not been fully elucidated. The 5-aminolevulinic acid (ALA)-based photodynamic action (PDA) was dependent on the accumulation of PpIX, the level of which decreased rapidly by eliminating ALA from the incubation medium in human Histiocytic Lymphoma U937 cells. PDA induced apoptosis characterized by lipid peroxidation, increase in Bak and Bax/Bcl-xL, decrease in Bid, membrane depolarization, cytochrome c release, caspase-3 activation, phosphatidylserine (PS) externalization. PDT-induced cell death seemed to occur predominantly via apoptosis through distribution of PpIX in mitochondria. These cell death events were enhanced by ferrochelatase inhibitors. These results indicated that ALA-based-PDA induced apoptotic cell death through a mitochondrial pathway and that ferrochelatase inhibitors might enhanced the effect of PDT for tumors even at low concentrations of ALA.
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regulation of 5 aminolevulinic acid dependent protoporphyrin ix accumulations in human Histiocytic Lymphoma u937 cells
Physiological chemistry and physics and medical NMR, 2007Co-Authors: Yuya Okimura, Keiji Inoue, Hirofumi Fujita, Taro Shuin, Tetsuya Ogino, Hiromi Yano, Tatsuji Yasuda, Masayasu Inoue, Kozo Utsumi, Junzo SasakiAbstract:The aim of the present work is to clarify the mechanism(s) that regulates the accumulation of protoporphyrin IX (PpIX) in human Histiocytic Lymphoma cell line U937 incubated with 5-aminolevulinic acid (ALA). Biosynthesis and accumulation of PpIX in the cells was determined after incubation with 0.1-5 mM ALA using a flow cytometric technique. The synthesized endogenous PpIX was found to localize predominantly in the mitochondrial region of the cells. The ALA-enhanced PpIX synthesis was suppressed by the presence of either beta-alanine, a competitive inhibitor of beta-transporters on cell membranes, or carbonyl cyanide p-trifluoromethoxyphenyl hydrazone, an uncoupler of mitochondrial oxidative phosphorylation. In contrast, cellular accumulation of PpIX was enhanced by the presence of either deferoxamine (an iron chelater), MnCl2 (a ferrochelatase inhibitor), or Sn-mesoporphyrin (heme oxygenase inhibitor). These results suggest that ALA-enhanced accumulation of PpIX in U937 cells was regulated by cellular uptake and conversion of ALA to PpIX and by degradation of Heme.
Keiji Inoue - One of the best experts on this subject based on the ideXlab platform.
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mechanism of cell death by 5 aminolevulinic acid based photodynamic action and its enhancement by ferrochelatase inhibitors in human Histiocytic Lymphoma cell line u937
Cell Biochemistry and Function, 2009Co-Authors: Takashi Amo, Keiji Inoue, Hirofumi Fujita, Noriaki Kawanishi, Masataka Uchida, Eri Oyanagi, Toshihiko Utsumi, Tetsuya Ogino, Taro ShuinAbstract:Photodynamic therapy (PDT) for tumors is based on the tumor-selective accumulation of a photosensitizer, protoporphyrin IX (PpIX), followed by irradiation with visible light. However, the molecular mechanism of cell death caused by PDT has not been fully elucidated. The 5-aminolevulinic acid (ALA)-based photodynamic action (PDA) was dependent on the accumulation of PpIX, the level of which decreased rapidly by eliminating ALA from the incubation medium in human Histiocytic Lymphoma U937 cells. PDA induced apoptosis characterized by lipid peroxidation, increase in Bak and Bax/Bcl-xL, decrease in Bid, membrane depolarization, cytochrome c release, caspase-3 activation, phosphatidylserine (PS) externalization. PDT-induced cell death seemed to occur predominantly via apoptosis through distribution of PpIX in mitochondria. These cell death events were enhanced by ferrochelatase inhibitors. These results indicated that ALA-based-PDA induced apoptotic cell death through a mitochondrial pathway and that ferrochelatase inhibitors might enhanced the effect of PDT for tumors even at low concentrations of ALA. Copyright © 2009 John Wiley & Sons, Ltd.
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mechanism of cell death by 5 aminolevulinic acid based photodynamic action and its enhancement by ferrochelatase inhibitors in human Histiocytic Lymphoma cell line u937
Cell Biochemistry and Function, 2009Co-Authors: Takashi Amo, Keiji Inoue, Hirofumi Fujita, Noriaki Kawanishi, Masataka Uchida, Eri Oyanagi, Toshihiko Utsumi, Tetsuya Ogino, Taro ShuinAbstract:Photodynamic therapy (PDT) for tumors is based on the tumor-selective accumulation of a photosensitizer, protoporphyrin IX (PpIX), followed by irradiation with visible light. However, the molecular mechanism of cell death caused by PDT has not been fully elucidated. The 5-aminolevulinic acid (ALA)-based photodynamic action (PDA) was dependent on the accumulation of PpIX, the level of which decreased rapidly by eliminating ALA from the incubation medium in human Histiocytic Lymphoma U937 cells. PDA induced apoptosis characterized by lipid peroxidation, increase in Bak and Bax/Bcl-xL, decrease in Bid, membrane depolarization, cytochrome c release, caspase-3 activation, phosphatidylserine (PS) externalization. PDT-induced cell death seemed to occur predominantly via apoptosis through distribution of PpIX in mitochondria. These cell death events were enhanced by ferrochelatase inhibitors. These results indicated that ALA-based-PDA induced apoptotic cell death through a mitochondrial pathway and that ferrochelatase inhibitors might enhanced the effect of PDT for tumors even at low concentrations of ALA.
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regulation of 5 aminolevulinic acid dependent protoporphyrin ix accumulations in human Histiocytic Lymphoma u937 cells
Physiological chemistry and physics and medical NMR, 2007Co-Authors: Yuya Okimura, Keiji Inoue, Hirofumi Fujita, Taro Shuin, Tetsuya Ogino, Hiromi Yano, Tatsuji Yasuda, Masayasu Inoue, Kozo Utsumi, Junzo SasakiAbstract:The aim of the present work is to clarify the mechanism(s) that regulates the accumulation of protoporphyrin IX (PpIX) in human Histiocytic Lymphoma cell line U937 incubated with 5-aminolevulinic acid (ALA). Biosynthesis and accumulation of PpIX in the cells was determined after incubation with 0.1-5 mM ALA using a flow cytometric technique. The synthesized endogenous PpIX was found to localize predominantly in the mitochondrial region of the cells. The ALA-enhanced PpIX synthesis was suppressed by the presence of either beta-alanine, a competitive inhibitor of beta-transporters on cell membranes, or carbonyl cyanide p-trifluoromethoxyphenyl hydrazone, an uncoupler of mitochondrial oxidative phosphorylation. In contrast, cellular accumulation of PpIX was enhanced by the presence of either deferoxamine (an iron chelater), MnCl2 (a ferrochelatase inhibitor), or Sn-mesoporphyrin (heme oxygenase inhibitor). These results suggest that ALA-enhanced accumulation of PpIX in U937 cells was regulated by cellular uptake and conversion of ALA to PpIX and by degradation of Heme.