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Article: Effects of N-acetylcysteine on nicotinamide dinucleotide phosphate oxidase activation and antioxidant status in heart, lung, liver and kidney in streptozotocin-induced diabetic rats
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TitleEffects of N-acetylcysteine on nicotinamide dinucleotide phosphate oxidase activation and antioxidant status in heart, lung, liver and kidney in streptozotocin-induced diabetic rats
 
AuthorsLei, S2 1
Liu, Y1
Liu, H1
Yu, H2
Wang, H2
Xia, Z2 1
 
Keywords15-F 2T-Isoprostane
Antioxidant Status
Diabetes
N-Acetylcysteine
Nadph Oxidase
 
Issue Date2012
 
CitationYonsei Medical Journal, 2012, v. 53 n. 2, p. 294-303 [How to Cite?]
DOI: http://dx.doi.org/10.3349/ymj.2012.53.2.294
 
AbstractPurpose: Hyperglycemia increases reactive oxygen species (ROS) and the resulting oxidative stress plays a key role in the pathogenesis of diabetic complications. Nicotinamide dinucleotide phosphate (NADPH) oxidase is one of the major sources of ROS production in diabetes. We, therefore, examined the possibility that NADPH oxidase activation is increased in various tissues, and that the antioxidant N-acetylcysteine (NAC) may have tissue specifc effects on NADPH oxidase and tissue antioxidant status in diabetes. Materials and Methods: Control (C) and streptozotocin-induced diabetic (D) rats were treated either with NAC (1.5 g/kg/ day) orally or placebo for 4 weeks. The plasma, heart, lung, liver, kidney were harvested immediately and stored for biochemical or immunoblot analysis. Results: levels of free 15-F 2t-isoprostane were increased in plasma, heart, lung, liver and kidney tissues in diabetic rats, accompanied with significantly increased membrane translocation of the NADPH oxidase subunit p67phox in all tissues and increased expression of the membrane-bound subunit p22phox in heart, lung and kidney. The tissue antioxidant activity in lung, liver and kidney was decreased in diabetic rats, while it was increased in heart tissue. NAC reduced the expression of p22phox and p67phox, suppressed p67phox membrane translocation, and reduced free 15-F 2t-isoprostane levels in all tissues. NAC increased antioxidant activity in liver and lung, but did not signifcantly affect antioxidant activity in heart and kidney. Conclusion: The current study shows that NAC inhibits NADPH oxidase activation in diabetes and attenuates tissue oxidative damage in all organs, even though its effects on antioxidant activity are tissue specifc. © Yonsei University College of Medicine 2012.
 
ISSN0513-5796
2013 Impact Factor: 1.263
2013 SCImago Journal Rankings: 0.495
 
DOIhttp://dx.doi.org/10.3349/ymj.2012.53.2.294
 
PubMed Central IDPMC3282981
 
ISI Accession Number IDWOS:000300213600008
Funding AgencyGrant Number
National Natural Science Foundation of China (NSFC)30872447
Research Grants Council of Hong Kong782910M
Funding Information:

This is supported by grant 30872447 from the National Natural Science Foundation of China (NSFC) and General Research Fund grants 782910M from Research Grants Council of Hong Kong.

 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorLei, S
 
dc.contributor.authorLiu, Y
 
dc.contributor.authorLiu, H
 
dc.contributor.authorYu, H
 
dc.contributor.authorWang, H
 
dc.contributor.authorXia, Z
 
dc.date.accessioned2012-05-29T06:01:17Z
 
dc.date.available2012-05-29T06:01:17Z
 
dc.date.issued2012
 
dc.description.abstractPurpose: Hyperglycemia increases reactive oxygen species (ROS) and the resulting oxidative stress plays a key role in the pathogenesis of diabetic complications. Nicotinamide dinucleotide phosphate (NADPH) oxidase is one of the major sources of ROS production in diabetes. We, therefore, examined the possibility that NADPH oxidase activation is increased in various tissues, and that the antioxidant N-acetylcysteine (NAC) may have tissue specifc effects on NADPH oxidase and tissue antioxidant status in diabetes. Materials and Methods: Control (C) and streptozotocin-induced diabetic (D) rats were treated either with NAC (1.5 g/kg/ day) orally or placebo for 4 weeks. The plasma, heart, lung, liver, kidney were harvested immediately and stored for biochemical or immunoblot analysis. Results: levels of free 15-F 2t-isoprostane were increased in plasma, heart, lung, liver and kidney tissues in diabetic rats, accompanied with significantly increased membrane translocation of the NADPH oxidase subunit p67phox in all tissues and increased expression of the membrane-bound subunit p22phox in heart, lung and kidney. The tissue antioxidant activity in lung, liver and kidney was decreased in diabetic rats, while it was increased in heart tissue. NAC reduced the expression of p22phox and p67phox, suppressed p67phox membrane translocation, and reduced free 15-F 2t-isoprostane levels in all tissues. NAC increased antioxidant activity in liver and lung, but did not signifcantly affect antioxidant activity in heart and kidney. Conclusion: The current study shows that NAC inhibits NADPH oxidase activation in diabetes and attenuates tissue oxidative damage in all organs, even though its effects on antioxidant activity are tissue specifc. © Yonsei University College of Medicine 2012.
 
dc.description.naturelink_to_OA_fulltext
 
dc.identifier.citationYonsei Medical Journal, 2012, v. 53 n. 2, p. 294-303 [How to Cite?]
DOI: http://dx.doi.org/10.3349/ymj.2012.53.2.294
 
dc.identifier.doihttp://dx.doi.org/10.3349/ymj.2012.53.2.294
 
dc.identifier.epage303
 
dc.identifier.hkuros204908
 
dc.identifier.isiWOS:000300213600008
Funding AgencyGrant Number
National Natural Science Foundation of China (NSFC)30872447
Research Grants Council of Hong Kong782910M
Funding Information:

This is supported by grant 30872447 from the National Natural Science Foundation of China (NSFC) and General Research Fund grants 782910M from Research Grants Council of Hong Kong.

 
dc.identifier.issn0513-5796
2013 Impact Factor: 1.263
2013 SCImago Journal Rankings: 0.495
 
dc.identifier.issue2
 
dc.identifier.pmcidPMC3282981
 
dc.identifier.pmid22318816
 
dc.identifier.scopuseid_2-s2.0-84863138767
 
dc.identifier.spage294
 
dc.identifier.urihttp://hdl.handle.net/10722/147290
 
dc.identifier.volume53
 
dc.languageeng
 
dc.relation.ispartofYonsei Medical Journal
 
dc.relation.referencesReferences in Scopus
 
dc.subject15-F 2T-Isoprostane
 
dc.subjectAntioxidant Status
 
dc.subjectDiabetes
 
dc.subjectN-Acetylcysteine
 
dc.subjectNadph Oxidase
 
dc.titleEffects of N-acetylcysteine on nicotinamide dinucleotide phosphate oxidase activation and antioxidant status in heart, lung, liver and kidney in streptozotocin-induced diabetic rats
 
dc.typeArticle
 
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<contributor.author>Wang, H</contributor.author>
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<description.abstract>Purpose: Hyperglycemia increases reactive oxygen species (ROS) and the resulting oxidative stress plays a key role in the pathogenesis of diabetic complications. Nicotinamide dinucleotide phosphate (NADPH) oxidase is one of the major sources of ROS production in diabetes. We, therefore, examined the possibility that NADPH oxidase activation is increased in various tissues, and that the antioxidant N-acetylcysteine (NAC) may have tissue specifc effects on NADPH oxidase and tissue antioxidant status in diabetes. Materials and Methods: Control (C) and streptozotocin-induced diabetic (D) rats were treated either with NAC (1.5 g/kg/ day) orally or placebo for 4 weeks. The plasma, heart, lung, liver, kidney were harvested immediately and stored for biochemical or immunoblot analysis. Results: levels of free 15-F 2t-isoprostane were increased in plasma, heart, lung, liver and kidney tissues in diabetic rats, accompanied with significantly increased membrane translocation of the NADPH oxidase subunit p67phox in all tissues and increased expression of the membrane-bound subunit p22phox in heart, lung and kidney. The tissue antioxidant activity in lung, liver and kidney was decreased in diabetic rats, while it was increased in heart tissue. NAC reduced the expression of p22phox and p67phox, suppressed p67phox membrane translocation, and reduced free 15-F 2t-isoprostane levels in all tissues. NAC increased antioxidant activity in liver and lung, but did not signifcantly affect antioxidant activity in heart and kidney. Conclusion: The current study shows that NAC inhibits NADPH oxidase activation in diabetes and attenuates tissue oxidative damage in all organs, even though its effects on antioxidant activity are tissue specifc. &#169; Yonsei University College of Medicine 2012.</description.abstract>
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Author Affiliations
  1. The University of Hong Kong
  2. Wuhan University