The Experts below are selected from a list of 14070 Experts worldwide ranked by ideXlab platform
Kevron Grant - One of the best experts on this subject based on the ideXlab platform.
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adenosine 5 phosphosulfate reductase apr2 mutation in arabidopsis implicates glutathione deficiency in selenate toxicity
Biochemical Journal, 2011Co-Authors: Kevron Grant, Nicole M Carey, Miguel Mendoza, John Schulze, Marinus Pilon, Elizabeth A H Pilonsmits, Doug Van HoewykAbstract:APR2 is the dominant APR (adenosine 5'-phosphosulfate reductase) in the model plant Arabidopsis thaliana, and converts activated sulfate to sulfite, a key reaction in the sulfate reduction pathway. To determine whether APR2 has a role in selenium tolerance and Metabolism, a mutant Arabidopsis line (apr2-1) was studied. apr2-1 plants had decreased selenate tolerance and photosynthetic efficiency. Sulfur Metabolism was perturbed in apr2-1 plants grown on selenate, as observed by an increase in total Sulfur and sulfate, and a 2-fold decrease in glutathione concentration. The altered Sulfur Metabolism in apr2-1 grown on selenate did not reflect typical sulfate starvation, as cysteine and methionine levels were increased. Knockout of APR2 also increased the accumulation of total selenium and selenate. However, the accumulation of selenite and selenium incorporation in protein was lower in apr2-1 mutants. Decreased incorporation of selenium in protein is typically associated with increased selenium tolerance in plants. However, because the apr2-1 mutant exhibited decreased tolerance to selenate, we propose that selenium toxicity can also be caused by selenate's disruption of glutathione biosynthesis leading to enhanced levels of damaging ROS (reactive oxygen species).
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adenosine 5 phosphosulfate reductase apr2 mutation in arabidopsis implicates glutathione deficiency in selenate toxicity
Biochemical Journal, 2011Co-Authors: Kevron Grant, Nicole M Carey, Miguel Mendoza, John Schulze, Marinus Pilon, Elizabeth A H Pilonsmits, Doug Van HoewykAbstract:�-phosphosulfate reductase) in the model plant Arabidopsis thaliana, and converts activated sulfate to sulfite, a key reaction in the sulfate reduction pathway. To determine whether APR2 has a role in selenium tolerance and Metabolism, a mutant Arabidopsis line (apr2-1) was studied. apr2-1 plants had decreased selenate tolerance and photosynthetic efficiency. Sulfur Metabolism was perturbed in apr2-1 plants grown on selenate, as observed by an increase in total Sulfur and sulfate, and a 2-fold decrease in glutathione concentration. The altered Sulfur Metabolism in apr2-1 grown on selenate did not reflect typical sulfate starvation, as cysteine and methionine levels were increased. Knockout of APR2 also increased the accumulation of total selenium and selenate. However,theaccumulationofseleniteandseleniumincorporation in protein was lower in apr2-1 mutants. Decreased incorporation of selenium in protein is typically associated with increased selenium tolerance in plants. However, because the apr2-1 mutant exhibited decreased tolerance to selenate, we propose that selenium toxicity can also be caused by selenate’s disruption of glutathione biosynthesis leading to enhanced levels of damaging ROS (reactive oxygen species).
Elizabeth A H Pilonsmits - One of the best experts on this subject based on the ideXlab platform.
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adenosine 5 phosphosulfate reductase apr2 mutation in arabidopsis implicates glutathione deficiency in selenate toxicity
Biochemical Journal, 2011Co-Authors: Kevron Grant, Nicole M Carey, Miguel Mendoza, John Schulze, Marinus Pilon, Elizabeth A H Pilonsmits, Doug Van HoewykAbstract:APR2 is the dominant APR (adenosine 5'-phosphosulfate reductase) in the model plant Arabidopsis thaliana, and converts activated sulfate to sulfite, a key reaction in the sulfate reduction pathway. To determine whether APR2 has a role in selenium tolerance and Metabolism, a mutant Arabidopsis line (apr2-1) was studied. apr2-1 plants had decreased selenate tolerance and photosynthetic efficiency. Sulfur Metabolism was perturbed in apr2-1 plants grown on selenate, as observed by an increase in total Sulfur and sulfate, and a 2-fold decrease in glutathione concentration. The altered Sulfur Metabolism in apr2-1 grown on selenate did not reflect typical sulfate starvation, as cysteine and methionine levels were increased. Knockout of APR2 also increased the accumulation of total selenium and selenate. However, the accumulation of selenite and selenium incorporation in protein was lower in apr2-1 mutants. Decreased incorporation of selenium in protein is typically associated with increased selenium tolerance in plants. However, because the apr2-1 mutant exhibited decreased tolerance to selenate, we propose that selenium toxicity can also be caused by selenate's disruption of glutathione biosynthesis leading to enhanced levels of damaging ROS (reactive oxygen species).
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adenosine 5 phosphosulfate reductase apr2 mutation in arabidopsis implicates glutathione deficiency in selenate toxicity
Biochemical Journal, 2011Co-Authors: Kevron Grant, Nicole M Carey, Miguel Mendoza, John Schulze, Marinus Pilon, Elizabeth A H Pilonsmits, Doug Van HoewykAbstract:�-phosphosulfate reductase) in the model plant Arabidopsis thaliana, and converts activated sulfate to sulfite, a key reaction in the sulfate reduction pathway. To determine whether APR2 has a role in selenium tolerance and Metabolism, a mutant Arabidopsis line (apr2-1) was studied. apr2-1 plants had decreased selenate tolerance and photosynthetic efficiency. Sulfur Metabolism was perturbed in apr2-1 plants grown on selenate, as observed by an increase in total Sulfur and sulfate, and a 2-fold decrease in glutathione concentration. The altered Sulfur Metabolism in apr2-1 grown on selenate did not reflect typical sulfate starvation, as cysteine and methionine levels were increased. Knockout of APR2 also increased the accumulation of total selenium and selenate. However,theaccumulationofseleniteandseleniumincorporation in protein was lower in apr2-1 mutants. Decreased incorporation of selenium in protein is typically associated with increased selenium tolerance in plants. However, because the apr2-1 mutant exhibited decreased tolerance to selenate, we propose that selenium toxicity can also be caused by selenate’s disruption of glutathione biosynthesis leading to enhanced levels of damaging ROS (reactive oxygen species).
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interactions between chromium and Sulfur Metabolism in brassica juncea
Journal of Environmental Quality, 2008Co-Authors: Michela Schiavon, Elizabeth A H Pilonsmits, Markus Wirtz, Riidiger Hell, Mario MalagoliAbstract:The effects of chromate on sulfate uptake and assimilation were investigated in the accumulator Brassica juncea (L.) Czern. Seven-day-old plants were grown for 2 d under the following combination of sulfate and chromate concentration: (i) no sulfate and no chromate (-S), (ii) no sulfate and 0.2 mmol L -1 chromate (-S +Cr), (iii) 1 mmol L -1 sulfate and no chromate (+S), or (iv) 1 mmol L -1 sulfate and 0.2 mmol L -1 chromate (+S +Cr). Despite the toxic effects exerted by chromate as indicated by altered level of reducing sugars and proteins in leaves, the growth of B. juncea was only weakly reduced by chromate, and no variation in chlorophyll a and b was measured, regardless of S availability. Chromium (Cr) was stored more in roots than in leaves, and the maximum Cr accumulation was measured in -S +Cr plants. The significant decrease of the sulfate uptake rates observed in Cr-treated plants was accompanied by a repression of the root low-affinity sulfate transporter (BjST1), suggesting that the transport of chromate in B. juncea may involve sulfate carriers. Once absorbed, chromate induced genes involved in sulfate assimilation (ATP-sulfarylase: atps6; APS-reductase: apsr2; Glutathione synthethase: gsh2) and accumulation of cysteine and glutathione, which may suggest that these reduced S compounds play a role in Cr tolerance. Together, our findings indicate that when phytoremediarion technologies are used to recover Cr-contaminated areas, the concentration of sulfate in the plant growth medium must be considered because it may influence the ability of plants to accumulate and tolerate Cr.
Kenneth N Maclean - One of the best experts on this subject based on the ideXlab platform.
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taurine treatment prevents derangement of the hepatic γ glutamyl cycle and methylglyoxal Metabolism in a mouse model of classical homocystinuria regulatory crosstalk between thiol and sulfinic acid Metabolism
The FASEB Journal, 2017Co-Authors: Kenneth N Maclean, Hua Jiang, Robert H Allen, Sally P Stabler, Stefanos Aivazidis, Eugene Kim, Colin T Shearn, Peter Harris, Dennis R Petersen, James R RoedeAbstract:Cystathionine β-synthase–deficient homocystinuria (HCU) is a poorly understood, life-threatening inborn error of Sulfur Metabolism. Analysis of hepatic glutathione (GSH) Metabolism in a mouse model...
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altered hepatic Sulfur Metabolism in cystathionine β synthase deficient homocystinuria regulatory role of taurine on competing cysteine oxidation pathways
The FASEB Journal, 2014Co-Authors: Hua Jiang, Robert H Allen, Sally P Stabler, Steven H Abman, Kenneth N MacleanAbstract:Cystathionine β-synthase-deficient homocystinuria (HCU) is a serious life-threatening inborn error of Sulfur Metabolism with poorly understood pathogenic mechanisms. We investigated the effect of HCU on hepatic cysteine oxidation in a transgenic mouse model of the disease. Cysteine dioxygenase (CDO) protein levels were 90% repressed without any change in mRNA levels. Cysteinesulfinic acid decarboxylase (CSAD) was induced at both the mRNA (8-fold) and protein (15-fold) levels. Cysteine supplementation normalized CDO protein levels without reversing the induction of CSAD. Regulatory changes in CDO and CSAD expression were proportional to homocysteine elevation, indicating a possible threshold effect. Hepatic and blood taurine levels in HCU animals were decreased by 21 and 35%, respectively, and normalized by cysteine supplementation. Expression of the cytoplasmic (GOT1) and mitochondrial (GOT2) isoforms of glutamic-oxaloacetic transaminase were repressed in HCU animals by 86 and 30%, respectively. HCU induc...
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altered hepatic Sulfur Metabolism in cystathionine β synthase deficient homocystinuria regulatory role of taurine on competing cysteine oxidation pathways
The FASEB Journal, 2014Co-Authors: Hua Jiang, Robert H Allen, Sally P Stabler, Steven H Abman, Kenneth N MacleanAbstract:Cystathionine β-synthase-deficient homocystinuria (HCU) is a serious life-threatening inborn error of Sulfur Metabolism with poorly understood pathogenic mechanisms. We investigated the effect of HCU on hepatic cysteine oxidation in a transgenic mouse model of the disease. Cysteine dioxygenase (CDO) protein levels were 90% repressed without any change in mRNA levels. Cysteinesulfinic acid decarboxylase (CSAD) was induced at both the mRNA (8-fold) and protein (15-fold) levels. Cysteine supplementation normalized CDO protein levels without reversing the induction of CSAD. Regulatory changes in CDO and CSAD expression were proportional to homocysteine elevation, indicating a possible threshold effect. Hepatic and blood taurine levels in HCU animals were decreased by 21 and 35%, respectively, and normalized by cysteine supplementation. Expression of the cytoplasmic (GOT1) and mitochondrial (GOT2) isoforms of glutamic-oxaloacetic transaminase were repressed in HCU animals by 86 and 30%, respectively. HCU induced regulatory changes in CSAD, CDO, and GOT1 expression were normalized by taurine supplementation, indicating that cysteine is not the only Sulfur compound that regulates hepatic cysteine oxidation. Collectively, our results indicate that HCU induces significant alterations of Sulfur Metabolism with the potential to contribute to pathogenesis and that cysteine and taurine have the potential to serve as adjunctive treatments in this disease.
Doug Van Hoewyk - One of the best experts on this subject based on the ideXlab platform.
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adenosine 5 phosphosulfate reductase apr2 mutation in arabidopsis implicates glutathione deficiency in selenate toxicity
Biochemical Journal, 2011Co-Authors: Kevron Grant, Nicole M Carey, Miguel Mendoza, John Schulze, Marinus Pilon, Elizabeth A H Pilonsmits, Doug Van HoewykAbstract:APR2 is the dominant APR (adenosine 5'-phosphosulfate reductase) in the model plant Arabidopsis thaliana, and converts activated sulfate to sulfite, a key reaction in the sulfate reduction pathway. To determine whether APR2 has a role in selenium tolerance and Metabolism, a mutant Arabidopsis line (apr2-1) was studied. apr2-1 plants had decreased selenate tolerance and photosynthetic efficiency. Sulfur Metabolism was perturbed in apr2-1 plants grown on selenate, as observed by an increase in total Sulfur and sulfate, and a 2-fold decrease in glutathione concentration. The altered Sulfur Metabolism in apr2-1 grown on selenate did not reflect typical sulfate starvation, as cysteine and methionine levels were increased. Knockout of APR2 also increased the accumulation of total selenium and selenate. However, the accumulation of selenite and selenium incorporation in protein was lower in apr2-1 mutants. Decreased incorporation of selenium in protein is typically associated with increased selenium tolerance in plants. However, because the apr2-1 mutant exhibited decreased tolerance to selenate, we propose that selenium toxicity can also be caused by selenate's disruption of glutathione biosynthesis leading to enhanced levels of damaging ROS (reactive oxygen species).
Doug Van Hoewyk - One of the best experts on this subject based on the ideXlab platform.
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adenosine 5 phosphosulfate reductase apr2 mutation in arabidopsis implicates glutathione deficiency in selenate toxicity
Biochemical Journal, 2011Co-Authors: Kevron Grant, Nicole M Carey, Miguel Mendoza, John Schulze, Marinus Pilon, Elizabeth A H Pilonsmits, Doug Van HoewykAbstract:�-phosphosulfate reductase) in the model plant Arabidopsis thaliana, and converts activated sulfate to sulfite, a key reaction in the sulfate reduction pathway. To determine whether APR2 has a role in selenium tolerance and Metabolism, a mutant Arabidopsis line (apr2-1) was studied. apr2-1 plants had decreased selenate tolerance and photosynthetic efficiency. Sulfur Metabolism was perturbed in apr2-1 plants grown on selenate, as observed by an increase in total Sulfur and sulfate, and a 2-fold decrease in glutathione concentration. The altered Sulfur Metabolism in apr2-1 grown on selenate did not reflect typical sulfate starvation, as cysteine and methionine levels were increased. Knockout of APR2 also increased the accumulation of total selenium and selenate. However,theaccumulationofseleniteandseleniumincorporation in protein was lower in apr2-1 mutants. Decreased incorporation of selenium in protein is typically associated with increased selenium tolerance in plants. However, because the apr2-1 mutant exhibited decreased tolerance to selenate, we propose that selenium toxicity can also be caused by selenate’s disruption of glutathione biosynthesis leading to enhanced levels of damaging ROS (reactive oxygen species).
