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Peroxiredoxin III and Sulfiredoxin Together Protect Mice from Pyrazole-Induced Oxidative Liver Injury

DC FieldValueLanguage
dc.contributor.author길인섭-
dc.contributor.author배수한-
dc.contributor.author성수행-
dc.contributor.author이서구-
dc.date.accessioned2014-12-19T16:28:07Z-
dc.date.available2014-12-19T16:28:07Z-
dc.date.issued2012-
dc.identifier.issn1523-0864-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/89584-
dc.description.abstractAims: To define the mechanisms underlying pyrazole-induced oxidative stress and the protective role of peroxiredoxins (Prxs) and sulfiredoxin (Srx) against such stress. Results: Pyrazole increased Srx expression in the liver of mice in a nuclear factor erythroid 2–related factor 2 (Nrf2)-dependent manner and induced Srx translocation from the cytosol to the endoplasmic reticulum (ER) and mitochondria. Pyrazole also induced the expression of CYP2E1, a primary reactive oxygen species (ROS) source for ethanol-induced liver injury, in ER and mitochondria. However, increased CYP2E1 levels only partially accounted for the pyrazole-mediated induction of Srx, prompting the investigation of CYP2E1-independent ROS generation downstream of pyrazole. Indeed, pyrazole increased ER stress, which is known to elevate mitochondrial ROS. In addition, pyrazole up-regulated CYP2E1 to a greater extent in mitochondria than in ER. Accordingly, among Prxs I to IV, PrxIII, which is localized to mitochondria, was preferentially hyperoxidized in the liver of pyrazole-treated mice. Pyrazole-induced oxidative damage to the liver was greater in PrxIII−/− mice than in wild-type mice. Such damage was also increased in Srx−/− mice treated with pyrazole, underscoring the role of Srx as the guardian of PrxIII. Innovation: The roles of Prxs, Srx, and ER stress have not been previously studied in relation to pyrazole toxicity. Conclusion: The concerted action of PrxIII and Srx is important for protection against pyrazole-induced oxidative stress arising from the convergent induction of CYP2E1-derived and ER stress-derived ROS in mitochondria.-
dc.description.statementOfResponsibilityopen-
dc.relation.isPartOfANTIOXIDANTS & REDOX SIGNALING-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAnimals-
dc.subject.MESHChemical and Drug Induced Liver Injury/genetics-
dc.subject.MESHChemical and Drug Induced Liver Injury/metabolism*-
dc.subject.MESHMale-
dc.subject.MESHMice-
dc.subject.MESHMice, Inbred C57BL-
dc.subject.MESHNF-E2-Related Factor 2/genetics-
dc.subject.MESHNF-E2-Related Factor 2/metabolism-
dc.subject.MESHOxidation-Reduction-
dc.subject.MESHOxidoreductases Acting on Sulfur Group Donors/genetics-
dc.subject.MESHOxidoreductases Acting on Sulfur Group Donors/metabolism*-
dc.subject.MESHPeroxiredoxin III/genetics-
dc.subject.MESHPeroxiredoxin III/metabolism*-
dc.subject.MESHPyrazoles/toxicity*-
dc.titlePeroxiredoxin III and Sulfiredoxin Together Protect Mice from Pyrazole-Induced Oxidative Liver Injury-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Life Science (의생명과학부)-
dc.contributor.googleauthorSoo Han Bae-
dc.contributor.googleauthorSu Haeng Sung-
dc.contributor.googleauthorHye Eun Lee-
dc.contributor.googleauthorHa Tan Kang-
dc.contributor.googleauthorSe Kyoung Lee-
dc.contributor.googleauthorSue Young Oh-
dc.contributor.googleauthorHyun Ae Woo In Sup Kil-
dc.contributor.googleauthorSue Goo Rhee-
dc.identifier.doi22490042-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA00281-
dc.contributor.localIdA01798-
dc.contributor.localIdA01948-
dc.contributor.localIdA02847-
dc.relation.journalcodeJ00190-
dc.identifier.eissn1557-7716-
dc.identifier.pmid22490042-
dc.subject.keywordAnimals-
dc.subject.keywordChemical and Drug Induced Liver Injury/genetics-
dc.subject.keywordChemical and Drug Induced Liver Injury/metabolism*-
dc.subject.keywordMale-
dc.subject.keywordMice-
dc.subject.keywordMice, Inbred C57BL-
dc.subject.keywordNF-E2-Related Factor 2/genetics-
dc.subject.keywordNF-E2-Related Factor 2/metabolism-
dc.subject.keywordOxidation-Reduction-
dc.subject.keywordOxidoreductases Acting on Sulfur Group Donors/genetics-
dc.subject.keywordOxidoreductases Acting on Sulfur Group Donors/metabolism*-
dc.subject.keywordPeroxiredoxin III/genetics-
dc.subject.keywordPeroxiredoxin III/metabolism*-
dc.subject.keywordPyrazoles/toxicity*-
dc.contributor.alternativeNameKil, In Sup-
dc.contributor.alternativeNameBae, Soo Han-
dc.contributor.alternativeNameSung, Su Haeng-
dc.contributor.alternativeNameRhee, Sue Goo-
dc.contributor.affiliatedAuthorKil, In Sup-
dc.contributor.affiliatedAuthorBae, Soo Han-
dc.contributor.affiliatedAuthorSung, Su Haeng-
dc.contributor.affiliatedAuthorRhee, Sue Goo-
dc.citation.volume17-
dc.citation.number10-
dc.citation.startPage1351-
dc.citation.endPage1361-
dc.identifier.bibliographicCitationANTIOXIDANTS & REDOX SIGNALING, Vol.17(10) : 1351-1361, 2012-
Appears in Collections:
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers

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