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Conference Paper: Contribution of polyol pathway to diabetes-induced oxidative stress

TitleContribution of polyol pathway to diabetes-induced oxidative stress
Authors
Issue Date2003
PublisherAmerican Society of Nephrology. The Journal's web site is located at http://www.jasn.org
Citation
4th Hyonam Kidney Laboratory International Diabetes Symposium, Seoul, South Korea, 18-19 January 2003. In Journal Of The American Society Of Nephrology, 2003, v. 14 suppl. 3, p. S233-S236 How to Cite?
AbstractDiabetes causes increased oxidative stress, which is thought to play an important role in the pathogenesis of various diabetic complications. However, the source of the hyperglycemia-induced oxidative stress is not clear. It was found that the polyol pathway is the major contributor to oxidative stress in the lenses and nerves of diabetic mice. The first enzyme in the pathway, aldose reductase (AR), reduces glucose to sorbitol, which is then converted to fructose by sorbitol dehydrogenase (SDH). Transgenic mice that overexpress AR specifically in their lenses showed a significant increase in oxidative stress when they became hyperglycemic, as indicated by a decrease in GSH and an increase in malondialdehyde in their lenses. Introducing an SDH-deficient mutation into these transgenic mice significantly normalized the GSH and malondialdehyde levels. These results indicate that both enzymes of the polyol pathway contributed to hyperglycemia-induced oxidative stress in the lens. In the wild-type mice, diabetes caused a significant decrease in GSH in their sciatic nerves, indicative of oxidative stress. In the AR null mutant mice, diabetes did not lead to any decrease in the nerve GSH level. These results indicate that similar to the situation in the lens, AR is also the major contributor to hyperglycemia-induced oxidative stress in the nerve. Although increased flux of glucose through the polyol pathway leads to diabetic lesions in both the lenses and nerve, the mechanisms may be different. AR-induced osmotic stress seems to be the cause of diabetic cataract, whereas AR-induced oxidative stress is probably the cause of neuronal dysfunction.
Persistent Identifierhttp://hdl.handle.net/10722/78103
ISSN
2015 Impact Factor: 8.491
2015 SCImago Journal Rankings: 4.699
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChung, SSMen_HK
dc.contributor.authorHo, ECMen_HK
dc.contributor.authorLam, KSLen_HK
dc.contributor.authorChung, SKen_HK
dc.date.accessioned2010-09-06T07:39:12Z-
dc.date.available2010-09-06T07:39:12Z-
dc.date.issued2003en_HK
dc.identifier.citation4th Hyonam Kidney Laboratory International Diabetes Symposium, Seoul, South Korea, 18-19 January 2003. In Journal Of The American Society Of Nephrology, 2003, v. 14 suppl. 3, p. S233-S236en_HK
dc.identifier.issn1046-6673en_HK
dc.identifier.urihttp://hdl.handle.net/10722/78103-
dc.description.abstractDiabetes causes increased oxidative stress, which is thought to play an important role in the pathogenesis of various diabetic complications. However, the source of the hyperglycemia-induced oxidative stress is not clear. It was found that the polyol pathway is the major contributor to oxidative stress in the lenses and nerves of diabetic mice. The first enzyme in the pathway, aldose reductase (AR), reduces glucose to sorbitol, which is then converted to fructose by sorbitol dehydrogenase (SDH). Transgenic mice that overexpress AR specifically in their lenses showed a significant increase in oxidative stress when they became hyperglycemic, as indicated by a decrease in GSH and an increase in malondialdehyde in their lenses. Introducing an SDH-deficient mutation into these transgenic mice significantly normalized the GSH and malondialdehyde levels. These results indicate that both enzymes of the polyol pathway contributed to hyperglycemia-induced oxidative stress in the lens. In the wild-type mice, diabetes caused a significant decrease in GSH in their sciatic nerves, indicative of oxidative stress. In the AR null mutant mice, diabetes did not lead to any decrease in the nerve GSH level. These results indicate that similar to the situation in the lens, AR is also the major contributor to hyperglycemia-induced oxidative stress in the nerve. Although increased flux of glucose through the polyol pathway leads to diabetic lesions in both the lenses and nerve, the mechanisms may be different. AR-induced osmotic stress seems to be the cause of diabetic cataract, whereas AR-induced oxidative stress is probably the cause of neuronal dysfunction.en_HK
dc.languageengen_HK
dc.publisherAmerican Society of Nephrology. The Journal's web site is located at http://www.jasn.orgen_HK
dc.relation.ispartofJournal of the American Society of Nephrologyen_HK
dc.subject.meshAldehyde Reductase - metabolismen_HK
dc.subject.meshDiabetes Mellitus - metabolismen_HK
dc.subject.meshHumansen_HK
dc.subject.meshL-Iditol 2-Dehydrogenase - metabolismen_HK
dc.subject.meshLens, Crystalline - metabolismen_HK
dc.subject.meshNervous System - metabolismen_HK
dc.subject.meshOxidative Stressen_HK
dc.titleContribution of polyol pathway to diabetes-induced oxidative stressen_HK
dc.typeConference_Paperen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1046-6673&volume=14&issue=Suppl 3&spage=S233&epage=36&date=2003&atitle=Contribution+of+polyol+pathway+to+diabetes-induced+oxidative+stressen_HK
dc.identifier.emailChung, SSM: smchung@hkucc.hku.hken_HK
dc.identifier.emailLam, KSL: ksllam@hku.hken_HK
dc.identifier.emailChung, SK: skchung@hkucc.hku.hken_HK
dc.identifier.authorityChung, SSM=rp00376en_HK
dc.identifier.authorityLam, KSL=rp00343en_HK
dc.identifier.authorityChung, SK=rp00381en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.pmid12874437-
dc.identifier.scopuseid_2-s2.0-0042867413en_HK
dc.identifier.hkuros79339en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0042867413&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume14en_HK
dc.identifier.issuesuppl. 3en_HK
dc.identifier.spageS233en_HK
dc.identifier.epageS236en_HK
dc.identifier.isiWOS:000184430000006-
dc.publisher.placeUnited Statesen_HK
dc.description.other4th Hyonam Kidney Laboratory International Diabetes Symposium, Seoul, South Korea, 18-19 January 2003. In Journal Of The American Society Of Nephrology, 2003, v. 14 suppl. 3, p. S233-S236-
dc.identifier.scopusauthoridChung, SSM=14120761600en_HK
dc.identifier.scopusauthoridHo, ECM=14028314400en_HK
dc.identifier.scopusauthoridLam, KSL=8082870600en_HK
dc.identifier.scopusauthoridChung, SK=7404292976en_HK
dc.customcontrol.immutablecsl 160525-

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