File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Damage to macrophages by tert-butyl hydroperoxide and the protective action of the protein bound polysaccharide krestin

TitleDamage to macrophages by tert-butyl hydroperoxide and the protective action of the protein bound polysaccharide krestin
Authors
KeywordsGlutathione Peroxidase
Macrophage
Manganese Superoxide Dismutase
Non-Selenium Dependent Glutathione Peroxidase
Polysaccharide Krestin
Selenium Dependent Glutathione Peroxidase
Tert-Butyl Hydroperoxide
Issue Date1997
PublisherChapman & Hall, Journals Department. The Journal's web site is located at http://www.chaphall.com/chaphall/journals.html
Citation
Medical Science Research, 1997, v. 25 n. 9, p. 601-606 How to Cite?
AbstractPrevious work has shown that lipoperoxidative damage to macrophages caused by oxidatively modified low-density lipoprotein (O-LDL) plays an important role in foam cell formation, and that the polysaccharide krestin (PSK), a protein-bound polysaccharide extracted from Coriolus versicolor, can protect macrophages from foam cell formation caused by O-LDL and from damage to physiological functions induced by tert-butyl hydroperoxide (tbOOH). In order to demonstrate further the mechanism of lipoperoxidative damage in foam cell formation caused by O-LDL, we investigated the damage to macrophage ultrastructure induced by tbOOH, protection by PSK and its action mechanism. Macrophages incubated with tbOOH showed morphological changes under the transmission electron and scanning electron microscope, their survival rate was decreased markedly, and the effects could be prevented and alleviated by PSK. As compared with a non-PSK treated group, selenium dependent glutathione peroxidase (SeGSHPx) and non-selenium dependent glutathione peroxidase (non-SeGSHPx) activities, manganese superoxide dismutase (MnSOD) activity and mRNA content increased significantly in the PSK-treated group. These findings and previous studies taken together suggest that protection by PSK is due to the induction of gene expression of antioxidative enzymes, SeGSHPx, non-SeGSHPx and MnSOD, in the macrophages.
Persistent Identifierhttp://hdl.handle.net/10722/178602
ISSN
2001 Impact Factor: 0.384
2003 SCImago Journal Rankings: 0.107
References

 

DC FieldValueLanguage
dc.contributor.authorChen, Yen_US
dc.contributor.authorZhou, Men_US
dc.contributor.authorGuo, Zen_US
dc.contributor.authorLiu, Sen_US
dc.contributor.authorPang, Zen_US
dc.contributor.authorSun, Jen_US
dc.contributor.authorLou, Ken_US
dc.contributor.authorWan, Jen_US
dc.date.accessioned2012-12-19T09:48:37Z-
dc.date.available2012-12-19T09:48:37Z-
dc.date.issued1997en_US
dc.identifier.citationMedical Science Research, 1997, v. 25 n. 9, p. 601-606en_US
dc.identifier.issn0269-8951en_US
dc.identifier.urihttp://hdl.handle.net/10722/178602-
dc.description.abstractPrevious work has shown that lipoperoxidative damage to macrophages caused by oxidatively modified low-density lipoprotein (O-LDL) plays an important role in foam cell formation, and that the polysaccharide krestin (PSK), a protein-bound polysaccharide extracted from Coriolus versicolor, can protect macrophages from foam cell formation caused by O-LDL and from damage to physiological functions induced by tert-butyl hydroperoxide (tbOOH). In order to demonstrate further the mechanism of lipoperoxidative damage in foam cell formation caused by O-LDL, we investigated the damage to macrophage ultrastructure induced by tbOOH, protection by PSK and its action mechanism. Macrophages incubated with tbOOH showed morphological changes under the transmission electron and scanning electron microscope, their survival rate was decreased markedly, and the effects could be prevented and alleviated by PSK. As compared with a non-PSK treated group, selenium dependent glutathione peroxidase (SeGSHPx) and non-selenium dependent glutathione peroxidase (non-SeGSHPx) activities, manganese superoxide dismutase (MnSOD) activity and mRNA content increased significantly in the PSK-treated group. These findings and previous studies taken together suggest that protection by PSK is due to the induction of gene expression of antioxidative enzymes, SeGSHPx, non-SeGSHPx and MnSOD, in the macrophages.en_US
dc.languageengen_US
dc.publisherChapman & Hall, Journals Department. The Journal's web site is located at http://www.chaphall.com/chaphall/journals.htmlen_US
dc.relation.ispartofMedical Science Researchen_US
dc.subjectGlutathione Peroxidaseen_US
dc.subjectMacrophageen_US
dc.subjectManganese Superoxide Dismutaseen_US
dc.subjectNon-Selenium Dependent Glutathione Peroxidaseen_US
dc.subjectPolysaccharide Krestinen_US
dc.subjectSelenium Dependent Glutathione Peroxidaseen_US
dc.subjectTert-Butyl Hydroperoxideen_US
dc.titleDamage to macrophages by tert-butyl hydroperoxide and the protective action of the protein bound polysaccharide krestinen_US
dc.typeArticleen_US
dc.identifier.emailWan, J: jmfwan@hku.hken_US
dc.identifier.authorityWan, J=rp00798en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.scopuseid_2-s2.0-0030830092en_US
dc.identifier.hkuros35641-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0030830092&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume25en_US
dc.identifier.issue9en_US
dc.identifier.spage601en_US
dc.identifier.epage606en_US
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridChen, Y=16745998900en_US
dc.identifier.scopusauthoridZhou, M=7403506134en_US
dc.identifier.scopusauthoridGuo, Z=55227962300en_US
dc.identifier.scopusauthoridLiu, S=7409463469en_US
dc.identifier.scopusauthoridPang, Z=7103343225en_US
dc.identifier.scopusauthoridSun, J=35175139900en_US
dc.identifier.scopusauthoridLou, K=7006629613en_US
dc.identifier.scopusauthoridWan, J=8930305000en_US

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats