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Article: Contributions of polyol pathway to oxidative stress in diabetic cataract

TitleContributions of polyol pathway to oxidative stress in diabetic cataract
Authors
KeywordsAldose reductase
Glutathione
Malondialdehyde
Sorbitol dehydrogenase
Transgenic mice
Issue Date1999
PublisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/
Citation
Faseb Journal, 1999, v. 13 n. 1, p. 23-30 How to Cite?
AbstractThere is strong evidence to show that diabetes is associated with increased oxidative stress. However, the source of this oxidative stress remains unclear. Using transgenic mice that overexpress aldose reductase (AR) in their lenses, we found that the flux of glucose through the polyol pathway is the major cause of hyperglycemic oxidative stress in this tissue. The substantial decrease in the level of reduced glutathione (GSH) with concomitant rise in the level of lipid peroxidation product malondialdehyde (MDA) in the lens of transgenic mice, but not in the nontransgenic mice, suggests that glucose autoxidation and nonenzymatic glycation do not contribute significantly to oxidative stress in diabetic lenses. AR reduction of glucose to sorbitol probably contributes to oxidative stress by depleting its cofactor NADPH, which is also required for the regeneration of GSH. Sorbitol dehydrogenase, the second enzyme in the polyol pathway that converts sorbitol to fructose, also contributes to oxidative stress, most likely because depletion of its cofactor NAD + leads to more glucose being channeled through the polyol pathway. Despite a more than 100% increase of MDA, oxidative stress plays only a minor role in the development of cataract in this acute diabetic cataract model. However, chronic oxidative stress generated by the polyol pathway is likely to be an important contributing factor in the slow-developing diabetic cataract as well as in the development of other diabetic complications.
Persistent Identifierhttp://hdl.handle.net/10722/88044
ISSN
2015 Impact Factor: 5.299
2015 SCImago Journal Rankings: 2.775
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLee, AYWen_HK
dc.contributor.authorChung, SSMen_HK
dc.date.accessioned2010-09-06T09:37:55Z-
dc.date.available2010-09-06T09:37:55Z-
dc.date.issued1999en_HK
dc.identifier.citationFaseb Journal, 1999, v. 13 n. 1, p. 23-30en_HK
dc.identifier.issn0892-6638en_HK
dc.identifier.urihttp://hdl.handle.net/10722/88044-
dc.description.abstractThere is strong evidence to show that diabetes is associated with increased oxidative stress. However, the source of this oxidative stress remains unclear. Using transgenic mice that overexpress aldose reductase (AR) in their lenses, we found that the flux of glucose through the polyol pathway is the major cause of hyperglycemic oxidative stress in this tissue. The substantial decrease in the level of reduced glutathione (GSH) with concomitant rise in the level of lipid peroxidation product malondialdehyde (MDA) in the lens of transgenic mice, but not in the nontransgenic mice, suggests that glucose autoxidation and nonenzymatic glycation do not contribute significantly to oxidative stress in diabetic lenses. AR reduction of glucose to sorbitol probably contributes to oxidative stress by depleting its cofactor NADPH, which is also required for the regeneration of GSH. Sorbitol dehydrogenase, the second enzyme in the polyol pathway that converts sorbitol to fructose, also contributes to oxidative stress, most likely because depletion of its cofactor NAD + leads to more glucose being channeled through the polyol pathway. Despite a more than 100% increase of MDA, oxidative stress plays only a minor role in the development of cataract in this acute diabetic cataract model. However, chronic oxidative stress generated by the polyol pathway is likely to be an important contributing factor in the slow-developing diabetic cataract as well as in the development of other diabetic complications.en_HK
dc.languageengen_HK
dc.publisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/en_HK
dc.relation.ispartofFASEB Journalen_HK
dc.subjectAldose reductaseen_HK
dc.subjectGlutathioneen_HK
dc.subjectMalondialdehydeen_HK
dc.subjectSorbitol dehydrogenaseen_HK
dc.subjectTransgenic miceen_HK
dc.titleContributions of polyol pathway to oxidative stress in diabetic cataracten_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0892-6638&volume=13&spage=23&epage=30&date=1999&atitle=Contributions+of+polyol+pathway+to+oxidative+stress+in+diabetic+cataracten_HK
dc.identifier.emailChung, SSM: smchung@hkucc.hku.hken_HK
dc.identifier.authorityChung, SSM=rp00376en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.pmid9872926-
dc.identifier.scopuseid_2-s2.0-0032958288en_HK
dc.identifier.hkuros43897en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0032958288&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume13en_HK
dc.identifier.issue1en_HK
dc.identifier.spage23en_HK
dc.identifier.epage30en_HK
dc.identifier.isiWOS:000078029500003-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLee, AYW=55477259800en_HK
dc.identifier.scopusauthoridChung, SSM=14120761600en_HK

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