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| Description
| - Aims: To define the consequences of loss of cysteine dioxygenase (CDO) on cysteine metabolism at the tissue level, we determined levels of relevant metabolites and enzymes and evidence of H2S/HS- (gaseous hydrogen sulfide and its conjugate base) toxicity in liver, pancreas, kidney, and lung of CDO-/- mice that were fed either a taurine-free or taurine-supplemented diet. Results: CDO-/- mice had low tissue and serum taurine and hypotaurine levels and high tissue levels of cysteine, consistent with the loss of CDO. CDO-/- mice had elevated urinary excretion of thiosulfate, high tissue and serum cystathionine and lanthionine levels, and evidence of inhibition and destabilization of cytochrome c oxidase, which is consistent with excess production of H2S/HS-. Accumulation of cystathionine and lanthionine appeared to result from cystathionine -synthase (CBS)-mediated cysteine desulfhydration. Very high levels of hypotaurine in pancreas of wild-type mice and very high levels of cystathionine and lanthionine in pancreas of CDO-/- mice were observed, suggesting a unique cysteine metabolism in the pancreas. Innovation: The CDO-/- mouse model provides new insights into tissue-specific cysteine metabolism, particularly the role of pancreas in metabolism of excess cysteine by CBS-catalyzed reactions, and will be a useful model for studying the effects of excess endogenous production of H2S/HS-. Conclusion: The CDO-/- mouse clearly demonstrates that H2S/HS- production in tissues can exceed the capacity of the animal to oxidize sulfide to sulfate and demonstrates that pancreas and lung are more susceptible to toxicity from endogenous H2S/HS(-)production than are liver and kidney. Antioxid. Redox Signal. 19, 1321-1336.
- Aims: To define the consequences of loss of cysteine dioxygenase (CDO) on cysteine metabolism at the tissue level, we determined levels of relevant metabolites and enzymes and evidence of H2S/HS- (gaseous hydrogen sulfide and its conjugate base) toxicity in liver, pancreas, kidney, and lung of CDO-/- mice that were fed either a taurine-free or taurine-supplemented diet. Results: CDO-/- mice had low tissue and serum taurine and hypotaurine levels and high tissue levels of cysteine, consistent with the loss of CDO. CDO-/- mice had elevated urinary excretion of thiosulfate, high tissue and serum cystathionine and lanthionine levels, and evidence of inhibition and destabilization of cytochrome c oxidase, which is consistent with excess production of H2S/HS-. Accumulation of cystathionine and lanthionine appeared to result from cystathionine -synthase (CBS)-mediated cysteine desulfhydration. Very high levels of hypotaurine in pancreas of wild-type mice and very high levels of cystathionine and lanthionine in pancreas of CDO-/- mice were observed, suggesting a unique cysteine metabolism in the pancreas. Innovation: The CDO-/- mouse model provides new insights into tissue-specific cysteine metabolism, particularly the role of pancreas in metabolism of excess cysteine by CBS-catalyzed reactions, and will be a useful model for studying the effects of excess endogenous production of H2S/HS-. Conclusion: The CDO-/- mouse clearly demonstrates that H2S/HS- production in tissues can exceed the capacity of the animal to oxidize sulfide to sulfate and demonstrates that pancreas and lung are more susceptible to toxicity from endogenous H2S/HS(-)production than are liver and kidney. Antioxid. Redox Signal. 19, 1321-1336. (en)
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| Title
| - The Cysteine Dioxgenase Knockout Mouse: Altered Cysteine Metabolism in Nonhepatic Tissues Leads to Excess H2S/HS- Production and Evidence of Pancreatic and Lung Toxicity
- The Cysteine Dioxgenase Knockout Mouse: Altered Cysteine Metabolism in Nonhepatic Tissues Leads to Excess H2S/HS- Production and Evidence of Pancreatic and Lung Toxicity (en)
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| skos:prefLabel
| - The Cysteine Dioxgenase Knockout Mouse: Altered Cysteine Metabolism in Nonhepatic Tissues Leads to Excess H2S/HS- Production and Evidence of Pancreatic and Lung Toxicity
- The Cysteine Dioxgenase Knockout Mouse: Altered Cysteine Metabolism in Nonhepatic Tissues Leads to Excess H2S/HS- Production and Evidence of Pancreatic and Lung Toxicity (en)
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| skos:notation
| - RIV/00064165:_____/13:10193137!RIV14-MZ0-00064165
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| http://linked.open...avai/predkladatel
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| http://linked.open...avai/riv/aktivita
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| http://linked.open...avai/riv/aktivity
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| http://linked.open...iv/cisloPeriodika
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| http://linked.open...vai/riv/dodaniDat
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| http://linked.open...aciTvurceVysledku
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| http://linked.open.../riv/druhVysledku
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| http://linked.open...iv/duvernostUdaju
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| http://linked.open...titaPredkladatele
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| http://linked.open...dnocenehoVysledku
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| http://linked.open...ai/riv/idVysledku
| - RIV/00064165:_____/13:10193137
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| http://linked.open...riv/jazykVysledku
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| http://linked.open.../riv/klicovaSlova
| - system; enzymes; sulfur; amino-acids; dioxygenase gene; structural organization; ethylmalonic encephalopathy; taurine synthesis; hydrogen-sulfide metabolism; cystathionine beta-synthase (en)
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| http://linked.open.../riv/klicoveSlovo
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| http://linked.open...odStatuVydavatele
| - US - Spojené státy americké
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| http://linked.open...ontrolniKodProRIV
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| http://linked.open...i/riv/nazevZdroje
| - Antioxidants and Redox Signaling
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| http://linked.open...in/vavai/riv/obor
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| http://linked.open...ichTvurcuVysledku
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| http://linked.open...cetTvurcuVysledku
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| http://linked.open...UplatneniVysledku
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| http://linked.open...v/svazekPeriodika
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| http://linked.open...iv/tvurceVysledku
| - Kožich, Viktor
- Krijt, Jakub
- Hirschberger, Lawrence L.
- Roman, Heather B.
- Stipanuk, Martha H.
- Valli, Alessandro
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| http://linked.open...ain/vavai/riv/wos
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| issn
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| number of pages
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| http://bibframe.org/vocab/doi
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