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Article: Polyol pathway mediates iron-induced oxidative injury in ischemic-reperfused rat heart

TitlePolyol pathway mediates iron-induced oxidative injury in ischemic-reperfused rat heart
Authors
KeywordsFree radicals
Iron
Ischemia-reperfusion injury
Lipid peroxidation
Polyol pathway
Transferrin
Issue Date2008
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/freeradbiomed
Citation
Free Radical Biology And Medicine, 2008, v. 45 n. 5, p. 602-610 How to Cite?
AbstractRecent studies have shown that the polyol pathway is involved in ischemia-reperfusion (I/R)-induced myocardial infarction, but the mechanism is unclear. We previously found that lack of aldose reductase (AR), the first enzyme of the polyol pathway, attenuated the increase in transferrin (Tf) level in I/R brain, suggesting that AR contributes to iron-catalyzed free radical-induced damage. We therefore investigated if this mechanism occurs in I/R hearts. We found that inhibition of AR or sorbitol dehydrogenase (SDH), the second enzyme of the polyol pathway, both attenuated the I/R-mediated increases in HIF-1α, Tf, TfR, and intracellular iron content and reduced the I/R-induced infarct area of the heart. Further, administration of niacin, which replenishes NAD+, the cofactor for SDH, also normalized TfR and HIF-1α levels in I/R hearts. These results suggest that during I/R polyol pathway activity increases the cytosolic NADH/NAD+ ratio. This activates HIF-1α that induces the expression of TfR, which in turn increases Tf uptake and iron accumulation and exacerbates oxidative damage that increases the lipid peroxidation. This was confirmed by the fact that administration of the iron chelator deferoxamine attenuated the I/R-induced myocardial infarction. © 2008 Elsevier B.V. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/124482
ISSN
2015 Impact Factor: 5.784
2015 SCImago Journal Rankings: 2.468
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTang, WHen_HK
dc.contributor.authorWu, Sen_HK
dc.contributor.authorWong, TMen_HK
dc.contributor.authorChung, SKen_HK
dc.contributor.authorChung, SSMen_HK
dc.date.accessioned2010-10-31T10:36:52Z-
dc.date.available2010-10-31T10:36:52Z-
dc.date.issued2008en_HK
dc.identifier.citationFree Radical Biology And Medicine, 2008, v. 45 n. 5, p. 602-610en_HK
dc.identifier.issn0891-5849en_HK
dc.identifier.urihttp://hdl.handle.net/10722/124482-
dc.description.abstractRecent studies have shown that the polyol pathway is involved in ischemia-reperfusion (I/R)-induced myocardial infarction, but the mechanism is unclear. We previously found that lack of aldose reductase (AR), the first enzyme of the polyol pathway, attenuated the increase in transferrin (Tf) level in I/R brain, suggesting that AR contributes to iron-catalyzed free radical-induced damage. We therefore investigated if this mechanism occurs in I/R hearts. We found that inhibition of AR or sorbitol dehydrogenase (SDH), the second enzyme of the polyol pathway, both attenuated the I/R-mediated increases in HIF-1α, Tf, TfR, and intracellular iron content and reduced the I/R-induced infarct area of the heart. Further, administration of niacin, which replenishes NAD+, the cofactor for SDH, also normalized TfR and HIF-1α levels in I/R hearts. These results suggest that during I/R polyol pathway activity increases the cytosolic NADH/NAD+ ratio. This activates HIF-1α that induces the expression of TfR, which in turn increases Tf uptake and iron accumulation and exacerbates oxidative damage that increases the lipid peroxidation. This was confirmed by the fact that administration of the iron chelator deferoxamine attenuated the I/R-induced myocardial infarction. © 2008 Elsevier B.V. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/freeradbiomeden_HK
dc.relation.ispartofFree Radical Biology and Medicineen_HK
dc.subjectFree radicalsen_HK
dc.subjectIronen_HK
dc.subjectIschemia-reperfusion injuryen_HK
dc.subjectLipid peroxidationen_HK
dc.subjectPolyol pathwayen_HK
dc.subjectTransferrinen_HK
dc.subject.meshIron - metabolism-
dc.subject.meshMyocardial Reperfusion Injury - metabolism - pathology - prevention and control-
dc.subject.meshOxidative Stress-
dc.subject.meshPolymers - metabolism-
dc.subject.meshSignal Transduction-
dc.titlePolyol pathway mediates iron-induced oxidative injury in ischemic-reperfused rat hearten_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0891-5849&volume=45&spage=602&epage=610&date=2008&atitle=Polyol+pathway+mediates+iron-induced+oxidative+injury+in+ischemic-reperfused+rat+heart-
dc.identifier.emailChung, SK: skchung@hkucc.hku.hken_HK
dc.identifier.emailChung, SSM: smchung@hkucc.hku.hken_HK
dc.identifier.authorityChung, SK=rp00381en_HK
dc.identifier.authorityChung, SSM=rp00376en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.freeradbiomed.2008.05.003en_HK
dc.identifier.pmid18549825-
dc.identifier.scopuseid_2-s2.0-48449094505en_HK
dc.identifier.hkuros181690en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-48449094505&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume45en_HK
dc.identifier.issue5en_HK
dc.identifier.spage602en_HK
dc.identifier.epage610en_HK
dc.identifier.isiWOS:000258995200008-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridTang, WH=24399936100en_HK
dc.identifier.scopusauthoridWu, S=7408443898en_HK
dc.identifier.scopusauthoridWong, TM=7403531434en_HK
dc.identifier.scopusauthoridChung, SK=7404292976en_HK
dc.identifier.scopusauthoridChung, SSM=14120761600en_HK

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