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Article: Free cholesterol accumulation impairs antioxidant activities and aggravates apoptotic cell death in menadione-induced oxidative injury

TitleFree cholesterol accumulation impairs antioxidant activities and aggravates apoptotic cell death in menadione-induced oxidative injury
Authors
Lee, WSXu, MLi, YGu, YChen, JWong, DFung, PCWShen, J
KeywordsSuperoxide
Oxidative stress
Nitric oxide
Cholesterol
Apoptosis
Issue Date2011
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/yabbi
Citation
Archives of Biochemistry and Biophysics, 2011, v. 514 n. 1-2, p. 57-67 How to Cite?
DOI: http://dx.doi.org/10.1016/j.abb.2011.07.014
AbstractAlthough the relationship between hypercholesterolemia and oxidative stress has been extensively investigated, direct evidence regarding to the roles of cholesterol accumulation in the generations of reactive oxygen species (ROS) and apoptotic cell death under oxidative stress is lack. In this study, we investigated productions of superoxide anions (O(2)(-)) and nitric oxide (NO), and apoptotic cell death in wild type Chinese hamster ovary (CHO) cells and cholesterol accumulated CHO cells genetically and chemically. Oxidative stress was induced by menadione challenge. The results revealed that abundance of free cholesterol (FC) promoted menadione-induced O(2)(-) and NO productions. FC accumulation down-regulated eNOS expression but up-regulated NADPH oxidases, and inhibited the activities of superoxide dismutase (SOD) and catalase. Treatment of menadione increased the expressions of iNOS and qp91 phox, enhanced the activities of SOD and catalase in the wild-type CHO cells but inhibited the activity of glutathione peroxidase in the cholesterol accumulated CHO cells. Moreover, FC abundance promoted apoptotic cell death in these cells. Taken together, those results suggest that free cholesterol accumulation aggravates menadione-induced oxidative stress and exacerbates apoptotic cell death. © 2011 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/145565
ISSN
0003-9861
2023 Impact Factor: 3.8
2023 SCImago Journal Rankings: 0.888
ISI Accession Number ID
WOS:000295190900008
Funding AgencyGrant Number
RGC GRF774408M
749504M
University of Hong Kong
Funding Information:

This work was supported by RGC GRF Grants (774408M, 749504M) and Seed Fund for Basic Research, The University of Hong Kong. The authors would like to thank T.Y. Chang and Cathy C. Chang of Department of Biochemistry in Dartmouth Medical School for providing mutant CHO cells, reagents and technological instruction. The authors also thank Crystal Chueng of Department of Chemistry in The University of Hong Kong for her technological supports in EPR measurement.

References
References in Scopus

 

DC FieldValueLanguage
dc.contributor.authorLee, WSen_HK
dc.contributor.authorXu, Men_HK
dc.contributor.authorLi, Yen_HK
dc.contributor.authorGu, Yen_HK
dc.contributor.authorChen, Jen_HK
dc.contributor.authorWong, Den_HK
dc.contributor.authorFung, PCWen_HK
dc.contributor.authorShen, Jen_HK
dc.date.accessioned2012-02-28T01:54:53Z-
dc.date.available2012-02-28T01:54:53Z-
dc.date.issued2011en_HK
dc.identifier.citationArchives of Biochemistry and Biophysics, 2011, v. 514 n. 1-2, p. 57-67en_HK
dc.identifier.issn0003-9861en_HK
dc.identifier.urihttp://hdl.handle.net/10722/145565-
dc.description.abstractAlthough the relationship between hypercholesterolemia and oxidative stress has been extensively investigated, direct evidence regarding to the roles of cholesterol accumulation in the generations of reactive oxygen species (ROS) and apoptotic cell death under oxidative stress is lack. In this study, we investigated productions of superoxide anions (O(2)(-)) and nitric oxide (NO), and apoptotic cell death in wild type Chinese hamster ovary (CHO) cells and cholesterol accumulated CHO cells genetically and chemically. Oxidative stress was induced by menadione challenge. The results revealed that abundance of free cholesterol (FC) promoted menadione-induced O(2)(-) and NO productions. FC accumulation down-regulated eNOS expression but up-regulated NADPH oxidases, and inhibited the activities of superoxide dismutase (SOD) and catalase. Treatment of menadione increased the expressions of iNOS and qp91 phox, enhanced the activities of SOD and catalase in the wild-type CHO cells but inhibited the activity of glutathione peroxidase in the cholesterol accumulated CHO cells. Moreover, FC abundance promoted apoptotic cell death in these cells. Taken together, those results suggest that free cholesterol accumulation aggravates menadione-induced oxidative stress and exacerbates apoptotic cell death. © 2011 Elsevier Inc. All rights reserved.en_HK
dc.languageengen_US
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/yabbien_HK
dc.relation.ispartofArchives of Biochemistry and Biophysicsen_HK
dc.subjectSuperoxideen_HK
dc.subjectOxidative stressen_HK
dc.subjectNitric oxideen_HK
dc.subjectCholesterolen_HK
dc.subjectApoptosisen_HK
dc.subject.meshApoptosis - drug effects-
dc.subject.meshCholesterol - genetics - metabolism-
dc.subject.meshNitric Oxide - metabolism-
dc.subject.meshOxidative Stress - drug effects-
dc.subject.meshSuperoxides - metabolism-
dc.titleFree cholesterol accumulation impairs antioxidant activities and aggravates apoptotic cell death in menadione-induced oxidative injuryen_HK
dc.typeArticleen_HK
dc.identifier.emailLee, WS: waisin@hku.hken_HK
dc.identifier.emailLi, Y: liyuescm@hku.hken_HK
dc.identifier.emailChen, J: abchen@hku.hk-
dc.identifier.emailFung, PCW: hrspfcw@hku.hk-
dc.identifier.emailShen, J: shenjg@hku.hk-
dc.identifier.authorityChen, J=rp01316en_HK
dc.identifier.authorityShen, J=rp00487en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.abb.2011.07.014en_HK
dc.identifier.pmid21843500-
dc.identifier.scopuseid_2-s2.0-84860396107en_HK
dc.identifier.hkuros198771en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-84860396107&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume514en_HK
dc.identifier.issue1-2en_HK
dc.identifier.spage57en_HK
dc.identifier.epage67en_HK
dc.identifier.isiWOS:000295190900008-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridShen, J=7404929947en_HK
dc.identifier.scopusauthoridFung, PCW=7101613315en_HK
dc.identifier.scopusauthoridWong, D=55201834900en_HK
dc.identifier.scopusauthoridChen, J=22733695400en_HK
dc.identifier.scopusauthoridGu, Y=37014467100en_HK
dc.identifier.scopusauthoridLi, Y=36671636100en_HK
dc.identifier.scopusauthoridXu, M=54394643900en_HK
dc.identifier.scopusauthoridLee, W=12788473400en_HK
dc.identifier.citeulike9628084-
dc.identifier.issnl0003-9861-

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