Evidence map›Paper›PMID 23350603›Full record

ArticleAntioxidants & redox signaling2013

The cysteine dioxgenase knockout mouse: altered cysteine metabolism in nonhepatic tissues leads to excess H2S/HS(-) production and evidence of pancreatic and lung toxicity.

Heather B Roman, Lawrence L Hirschberger, Jakub Krijt, Alessandro Valli, Viktor Kožich, Martha H Stipanuk

Abstract read
In one paragraph

Article in Antioxidants & redox signaling, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
4.6field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

41 citing papers in PubMed, 68 citations in OpenAlex.

  1. Article
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  3. The Yin-Yang of sulfur dioxide: Effect on cognitive function.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review
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  9. Article
  10. The Journal of biological chemistry · 2019
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Environmental toxicology of hydrogen sulfide.Nitric oxide : biology and chemistry · 2017
    Review
  19. Review
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Heather B Roman1 Division of Nutritional Sciences, Cornell University , Ithaca, New York.
Lawrence L Hirschberger
Jakub Krijt
Alessandro Valli
Viktor Kožich
Martha H Stipanuk
Cornell University · US

Funding

NUTRITIONAL REGULATION OF CYSTEINE DIOXYGENASER01DK056649 · NIDDK · CORNELL UNIVERSITY ITHACA · PI STIPANUK, MARTHA H · 2000 to 2013
$4.0M
NIDDK NIH HHS DK-056649
6 · The paper itself

Abstract

aimsTo 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.

resultsCDO(-/-) 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 β-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(-).

conclusionThe 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.

Indexed as

AlanineAnimalsCystathionineCysteineCysteine DioxygenaseDietElectron Transport Complex IVEnzyme StabilityFemaleGlutathioneHydrogen SulfideKidneyLiverLungMaleMiceAlanineCystathionineCysteineCysteine DioxygenaseElectron Transport Complex IVGlutathioneHydrogen SulfidehypotaurinelanthionineSulfidesTaurine

Identifiers

PMID23350603
PMCPMC3791055
OpenAlexW2046015670

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.