The Experts below are selected from a list of 36024 Experts worldwide ranked by ideXlab platform
Stephen W. Tuttle - One of the best experts on this subject based on the ideXlab platform.
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effect of the k h ionophore nigericin on response of a549 cells to photodynamic therapy and tert butylhydroperoxide
Free Radical Biology and Medicine, 1993Co-Authors: Marie E. Varnes, Marian T. Bayne, Harry J. Menegay, Stephen W. TuttleAbstract:Abstract The K+/H+ ionophore negericin dramatically increases killing of V79 cells and A549 cells by photodynamic therapy (PDT) sensitized by chloroaluminum phthalocyanine. Previous studies suggested that the interaction between PDT and nigericin is related to the ability of this ionophore to reduce intracellular pH (pHi). The present study was undertaken to test the possibility that nigericin, by lowering pHi, inhibits reductive detoxification of PDT-produced peroxides by enzymes of the glutathione (GSH) redox cycle and the pentose cycle. To test this possibility we examined the effects of nigericin on the toxicity and metabolism of a model peroxide, tert-butylhydroperoxide (tert-BOOH), in A549 cells, a cell line in which the GSH redox cycle is known to be the Principal Pathway for reduction and detoxification of tert-BOOH. We found that nigericin equilibrates pHi of A549 cells with extracellular pH (pHe) in a time-dependent manner. It increases the toxicity of tert-BOOH toward A549 cells, inhibits loss of tert-BOOH from the buffer overlying the cells, and reduces the rate of 14CO2 release from radiolabelled glucose, which is measure of pentose cycle activity. These effects are significantly greater at pHe 6.40 than at 7.40. Monensin, a Na+/H+ ionophore which does not reduce pHi, does not enhance the toxicity of tert-BOOH and has only a minimal effect on tert-BOOH reduction. These data suggest that nigericin-induced inhibition of peroxide detoxification is at least a plausible mechanism by which the ionophore might interact with PDT.
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Effect of the K+/H+ ionophore nigericin on response of A549 cells to photodynamic therapy and tert-butylhydroperoxide.
Free radical biology & medicine, 1993Co-Authors: Marie E. Varnes, Marian T. Bayne, Harry J. Menegay, Stephen W. TuttleAbstract:Abstract The K+/H+ ionophore negericin dramatically increases killing of V79 cells and A549 cells by photodynamic therapy (PDT) sensitized by chloroaluminum phthalocyanine. Previous studies suggested that the interaction between PDT and nigericin is related to the ability of this ionophore to reduce intracellular pH (pHi). The present study was undertaken to test the possibility that nigericin, by lowering pHi, inhibits reductive detoxification of PDT-produced peroxides by enzymes of the glutathione (GSH) redox cycle and the pentose cycle. To test this possibility we examined the effects of nigericin on the toxicity and metabolism of a model peroxide, tert-butylhydroperoxide (tert-BOOH), in A549 cells, a cell line in which the GSH redox cycle is known to be the Principal Pathway for reduction and detoxification of tert-BOOH. We found that nigericin equilibrates pHi of A549 cells with extracellular pH (pHe) in a time-dependent manner. It increases the toxicity of tert-BOOH toward A549 cells, inhibits loss of tert-BOOH from the buffer overlying the cells, and reduces the rate of 14CO2 release from radiolabelled glucose, which is measure of pentose cycle activity. These effects are significantly greater at pHe 6.40 than at 7.40. Monensin, a Na+/H+ ionophore which does not reduce pHi, does not enhance the toxicity of tert-BOOH and has only a minimal effect on tert-BOOH reduction. These data suggest that nigericin-induced inhibition of peroxide detoxification is at least a plausible mechanism by which the ionophore might interact with PDT.
Joel C Glover - One of the best experts on this subject based on the ideXlab platform.
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Loss of Projections, Functional Compensation, and Residual Deficits in the Mammalian Vestibulospinal System of Hoxb1-Deficient Mice(1,2,3).
eNeuro, 2016Co-Authors: Maria Di Bonito, Jean-luc Boulland, Wojciech Krezel, Eya Setti, Michele Studer, Joel C GloverAbstract:The genetic mechanisms underlying the developmental and functional specification of brainstem projection neurons are poorly understood. Here, we use transgenic mouse tools to investigate the role of the gene Hoxb1 in the developmental patterning of vestibular projection neurons, with particular focus on the lateral vestibulospinal tract (LVST). The LVST is the Principal Pathway that conveys vestibular information to limb-related spinal motor circuits and arose early during vertebrate evolution. We show that the segmental hindbrain expression domain uniquely defined by the rhombomere 4 (r4) Hoxb1 enhancer is the origin of essentially all LVST neurons, but also gives rise to subpopulations of contralateral medial vestibulospinal tract (cMVST) neurons, vestibulo-ocular neurons, and reticulospinal (RS) neurons. In newborn mice homozygous for a Hoxb1-null mutation, the r4-derived LVST and cMVST subpopulations fail to form and the r4-derived RS neurons are depleted. Several general motor skills appear unimpaired, but hindlimb vestibulospinal reflexes, which are mediated by the LVST, are greatly reduced. This functional deficit recovers, however, during the second postnatal week, indicating a substantial compensation for the missing LVST. Despite the compensatory plasticity in balance, adult Hoxb1-null mice exhibit other behavioral deficits that manifest particularly in proprioception and interlimb coordination during locomotor tasks. Our results provide a comprehensive account of the developmental role of Hoxb1 in patterning the vestibular system and evidence for a remarkable developmental plasticity in the descending control of reflex limb movements. They also suggest an involvement of the lateral vestibulospinal tract in proprioception and in ensuring limb alternation generated by locomotor circuitry.
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Loss of Projections, Functional Compensation, and Residual Deficits in the Mammalian Vestibulospinal System of Hoxb1-Deficient Mice
eNeuro, 2015Co-Authors: Maria Di Bonito, Jean-luc Boulland, Wojciech Krezel, Eya Setti, Michele Studer, Joel C GloverAbstract:The genetic mechanisms underlying the developmental and functional specification of brainstem projection neurons are poorly understood. Here, we use transgenic mouse tools to investigate the role of the gene Hoxb1 in the developmental patterning of vestibular projection neurons, with particular focus on the lateral vestibulospinal tract (LVST). The LVST is the Principal Pathway that conveys vestibular information to limb-related spinal motor circuits and arose early during vertebrate evolution. We show that the segmental hindbrain expression domain uniquely defined by the rhombomere 4 (r4) Hoxb1 enhancer is the origin of essentially all LVST neurons, but also gives rise to subpopulations of contralateral medial vestibulospinal tract (cMVST) neurons, vestibulo-ocular neurons, and reticulospinal (RS) neurons. In newborn mice homozygous for a Hoxb1 -null mutation, the r4-derived LVST and cMVST subpopulations fail to form and the r4-derived RS neurons are depleted. Several general motor skills appear unimpaired, but hindlimb vestibulospinal reflexes, which are mediated by the LVST, are greatly reduced. This functional deficit recovers, however, during the second postnatal week, indicating a substantial compensation for the missing LVST. Despite the compensatory plasticity in balance, adult Hoxb1 -null mice exhibit other behavioral deficits that manifest particularly in proprioception and interlimb coordination during locomotor tasks. Our results provide a comprehensive account of the developmental role of Hoxb1 in patterning the vestibular system and evidence for a remarkable developmental plasticity in the descending control of reflex limb movements. They also suggest an involvement of the lateral vestibulospinal tract in proprioception and in ensuring limb alternation generated by locomotor circuitry.
Marie E. Varnes - One of the best experts on this subject based on the ideXlab platform.
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effect of the k h ionophore nigericin on response of a549 cells to photodynamic therapy and tert butylhydroperoxide
Free Radical Biology and Medicine, 1993Co-Authors: Marie E. Varnes, Marian T. Bayne, Harry J. Menegay, Stephen W. TuttleAbstract:Abstract The K+/H+ ionophore negericin dramatically increases killing of V79 cells and A549 cells by photodynamic therapy (PDT) sensitized by chloroaluminum phthalocyanine. Previous studies suggested that the interaction between PDT and nigericin is related to the ability of this ionophore to reduce intracellular pH (pHi). The present study was undertaken to test the possibility that nigericin, by lowering pHi, inhibits reductive detoxification of PDT-produced peroxides by enzymes of the glutathione (GSH) redox cycle and the pentose cycle. To test this possibility we examined the effects of nigericin on the toxicity and metabolism of a model peroxide, tert-butylhydroperoxide (tert-BOOH), in A549 cells, a cell line in which the GSH redox cycle is known to be the Principal Pathway for reduction and detoxification of tert-BOOH. We found that nigericin equilibrates pHi of A549 cells with extracellular pH (pHe) in a time-dependent manner. It increases the toxicity of tert-BOOH toward A549 cells, inhibits loss of tert-BOOH from the buffer overlying the cells, and reduces the rate of 14CO2 release from radiolabelled glucose, which is measure of pentose cycle activity. These effects are significantly greater at pHe 6.40 than at 7.40. Monensin, a Na+/H+ ionophore which does not reduce pHi, does not enhance the toxicity of tert-BOOH and has only a minimal effect on tert-BOOH reduction. These data suggest that nigericin-induced inhibition of peroxide detoxification is at least a plausible mechanism by which the ionophore might interact with PDT.
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Effect of the K+/H+ ionophore nigericin on response of A549 cells to photodynamic therapy and tert-butylhydroperoxide.
Free radical biology & medicine, 1993Co-Authors: Marie E. Varnes, Marian T. Bayne, Harry J. Menegay, Stephen W. TuttleAbstract:Abstract The K+/H+ ionophore negericin dramatically increases killing of V79 cells and A549 cells by photodynamic therapy (PDT) sensitized by chloroaluminum phthalocyanine. Previous studies suggested that the interaction between PDT and nigericin is related to the ability of this ionophore to reduce intracellular pH (pHi). The present study was undertaken to test the possibility that nigericin, by lowering pHi, inhibits reductive detoxification of PDT-produced peroxides by enzymes of the glutathione (GSH) redox cycle and the pentose cycle. To test this possibility we examined the effects of nigericin on the toxicity and metabolism of a model peroxide, tert-butylhydroperoxide (tert-BOOH), in A549 cells, a cell line in which the GSH redox cycle is known to be the Principal Pathway for reduction and detoxification of tert-BOOH. We found that nigericin equilibrates pHi of A549 cells with extracellular pH (pHe) in a time-dependent manner. It increases the toxicity of tert-BOOH toward A549 cells, inhibits loss of tert-BOOH from the buffer overlying the cells, and reduces the rate of 14CO2 release from radiolabelled glucose, which is measure of pentose cycle activity. These effects are significantly greater at pHe 6.40 than at 7.40. Monensin, a Na+/H+ ionophore which does not reduce pHi, does not enhance the toxicity of tert-BOOH and has only a minimal effect on tert-BOOH reduction. These data suggest that nigericin-induced inhibition of peroxide detoxification is at least a plausible mechanism by which the ionophore might interact with PDT.
Hideo Dohra - One of the best experts on this subject based on the ideXlab platform.
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Seasonal induction of alternative Principal Pathway for rose flower scent
Scientific reports, 2016Co-Authors: Hiroshi Hirata, Toshiyuki Ohnishi, Kensuke Tomida, Haruka Ishida, Momoyo Kanda, Miwa Sakai, Jin Yoshimura, Hideyuki Suzuki, Takamasa Ishikawa, Hideo DohraAbstract:Ecological adaptations to seasonal changes are often observed in the phenotypic traits of plants and animals, and these adaptations are usually expressed through the production of different biochemical end products. In this study, ecological adaptations are observed in a biochemical Pathway without alteration of the end products. We present an alternative Principal Pathway to the characteristic floral scent compound 2-phenylethanol (2PE) in roses. The new Pathway is seasonally induced in summer as a heat adaptation that uses rose phenylpyruvate decarboxylase (RyPPDC) as a novel enzyme. RyPPDC transcript levels and the resulting production of 2PE are increased time-dependently under high temperatures. The novel summer Pathway produces levels of 2PE that are several orders of magnitude higher than those produced by the previously known Pathway. Our results indicate that the alternative Principal Pathway identified here is a seasonal adaptation for managing the weakened volatility of summer roses.
Hiroshi Hirata - One of the best experts on this subject based on the ideXlab platform.
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Biosynthesis of floral scent 2-phenylethanol in rose flowers.
Bioscience Biotechnology and Biochemistry, 2016Co-Authors: Hiroshi Hirata, Toshiyuki Ohnishi, Naoharu WatanabeAbstract:Plants emit chemically diverse volatile compounds for attracting pollinators or putting up a chemical defense against herbivores. 2-Phenylethanol (2PE) is one of the abundantly emitted scent compounds in rose flowers. Feeding experiments with l-[2H8]phenylalanine into rose flowers and subsequent analysis using gas chromatography–mass spectrometry analysis revealed the hypothetical biosynthetic intermediates to [2H8]-2PE, and the biochemical and genetic analyses elucidated the Principal Pathway to [2H8]-2PE. We recently found season-specific 2PE Pathway producing [2H7]-2PE from l-[2H8]phenylalanine. This is a unique example where the dominant Pathway to a specific compound changes with the seasons. This review focuses on the biosynthesis of floral volatiles and their regulation to adapt to the changes in the environment.
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Seasonal induction of alternative Principal Pathway for rose flower scent
Scientific reports, 2016Co-Authors: Hiroshi Hirata, Toshiyuki Ohnishi, Kensuke Tomida, Haruka Ishida, Momoyo Kanda, Miwa Sakai, Jin Yoshimura, Hideyuki Suzuki, Takamasa Ishikawa, Hideo DohraAbstract:Ecological adaptations to seasonal changes are often observed in the phenotypic traits of plants and animals, and these adaptations are usually expressed through the production of different biochemical end products. In this study, ecological adaptations are observed in a biochemical Pathway without alteration of the end products. We present an alternative Principal Pathway to the characteristic floral scent compound 2-phenylethanol (2PE) in roses. The new Pathway is seasonally induced in summer as a heat adaptation that uses rose phenylpyruvate decarboxylase (RyPPDC) as a novel enzyme. RyPPDC transcript levels and the resulting production of 2PE are increased time-dependently under high temperatures. The novel summer Pathway produces levels of 2PE that are several orders of magnitude higher than those produced by the previously known Pathway. Our results indicate that the alternative Principal Pathway identified here is a seasonal adaptation for managing the weakened volatility of summer roses.