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Article: Relationship between glutathione S-transferase gene polymorphisms and enzyme activity in Hong Kong Chinese asthmatics

TitleRelationship between glutathione S-transferase gene polymorphisms and enzyme activity in Hong Kong Chinese asthmatics
Authors
Issue Date2007
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/CEA
Citation
Clinical And Experimental Allergy, 2007, v. 37 n. 8, p. 1150-1157 How to Cite?
AbstractBackground: Asthma is a disease associated with oxidative stress. The glutathione S-transferases (GST) are a group of enzymes that protect cells from oxidative stress. Functional genetic polymorphisms of GST genes (GSTT1, GSTM1 and GSTP1) have previously been reported. Objective: To investigate the association of GST gene polymorphisms and its enzyme activity with the risk of asthma in Hong Kong Chinese adults. Methods: An age- and smoking status-matched case-control study was carried out on 315 patients with asthma and 315 healthy controls. Genotyping was carried out on genomic DNA using the PCR and/or restriction fragment length polymorphism (PCR-RFLP). Plasma GST activity was measured by fluorometric assay. Results: The distribution of various genotypes or alleles of the GSTT1, GSTM1 and GSTP1 was not significantly different between patients with asthma and healthy controls. The GSTM1 null genotype was found to be protective from the development of asthma in atopic subjects (odds ratios 0.55, 95% confidence interval 0.34-0.90; P=0.017). However, there was no association between GSTT1 and GSTM1 null genotypes and enzyme activity. GSTP1 codon 105 Val variants led to reduced plasma GST activity in healthy controls. Asthma patients had elevated plasma GST activity compared with healthy controls irrespective of their genotypes (P<0.001). Conclusion: Our data suggest that among atopic subjects, the GSTM1 null genotype is associated with a decreased risk for asthma despite increased level of plasma GST activity in asthma, but it could not distinguish whether this increase is a potentially protective compensatory effect or a pathogenic factor. © 2007 Blackwell Publishing Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/77016
ISSN
2015 Impact Factor: 5.587
2015 SCImago Journal Rankings: 2.184
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorMak, JCWen_HK
dc.contributor.authorHo, SPen_HK
dc.contributor.authorLeung, HCMen_HK
dc.contributor.authorCheung, AHKen_HK
dc.contributor.authorLaw, BKWen_HK
dc.contributor.authorSo, LKYen_HK
dc.contributor.authorChan, JWMen_HK
dc.contributor.authorChau, CHen_HK
dc.contributor.authorLam, WKen_HK
dc.contributor.authorIp, MSMen_HK
dc.contributor.authorChanYeung, Men_HK
dc.date.accessioned2010-09-06T07:27:22Z-
dc.date.available2010-09-06T07:27:22Z-
dc.date.issued2007en_HK
dc.identifier.citationClinical And Experimental Allergy, 2007, v. 37 n. 8, p. 1150-1157en_HK
dc.identifier.issn0954-7894en_HK
dc.identifier.urihttp://hdl.handle.net/10722/77016-
dc.description.abstractBackground: Asthma is a disease associated with oxidative stress. The glutathione S-transferases (GST) are a group of enzymes that protect cells from oxidative stress. Functional genetic polymorphisms of GST genes (GSTT1, GSTM1 and GSTP1) have previously been reported. Objective: To investigate the association of GST gene polymorphisms and its enzyme activity with the risk of asthma in Hong Kong Chinese adults. Methods: An age- and smoking status-matched case-control study was carried out on 315 patients with asthma and 315 healthy controls. Genotyping was carried out on genomic DNA using the PCR and/or restriction fragment length polymorphism (PCR-RFLP). Plasma GST activity was measured by fluorometric assay. Results: The distribution of various genotypes or alleles of the GSTT1, GSTM1 and GSTP1 was not significantly different between patients with asthma and healthy controls. The GSTM1 null genotype was found to be protective from the development of asthma in atopic subjects (odds ratios 0.55, 95% confidence interval 0.34-0.90; P=0.017). However, there was no association between GSTT1 and GSTM1 null genotypes and enzyme activity. GSTP1 codon 105 Val variants led to reduced plasma GST activity in healthy controls. Asthma patients had elevated plasma GST activity compared with healthy controls irrespective of their genotypes (P<0.001). Conclusion: Our data suggest that among atopic subjects, the GSTM1 null genotype is associated with a decreased risk for asthma despite increased level of plasma GST activity in asthma, but it could not distinguish whether this increase is a potentially protective compensatory effect or a pathogenic factor. © 2007 Blackwell Publishing Ltd.en_HK
dc.languageengen_HK
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/CEAen_HK
dc.relation.ispartofClinical and Experimental Allergyen_HK
dc.rightsClinical and Experimental Allergy. Copyright © Blackwell Publishing Ltd.en_HK
dc.subject.meshAdulten_HK
dc.subject.meshAsian Continental Ancestry Groupen_HK
dc.subject.meshAsthma - blood - geneticsen_HK
dc.subject.meshCase-Control Studiesen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGenetic Predisposition to Diseaseen_HK
dc.subject.meshGenotypeen_HK
dc.subject.meshGlutathione Transferase - blood - geneticsen_HK
dc.subject.meshHong Kongen_HK
dc.subject.meshHumansen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshOxidative Stress - geneticsen_HK
dc.subject.meshPolymorphism, Restriction Fragment Lengthen_HK
dc.titleRelationship between glutathione S-transferase gene polymorphisms and enzyme activity in Hong Kong Chinese asthmaticsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0954-7894&volume=37&spage=1150&epage=1157&date=2007&atitle=Relationship+between+glutathione+S-transferase+gene+polymorphisms+and+enzyme+activity+in+Hong+Kong+Chinese+asthmaticsen_HK
dc.identifier.emailMak, JCW:judymak@hku.hken_HK
dc.identifier.emailIp, MSM:msmip@hku.hken_HK
dc.identifier.authorityMak, JCW=rp00352en_HK
dc.identifier.authorityIp, MSM=rp00347en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1365-2222.2007.02704.xen_HK
dc.identifier.pmid17651144en_HK
dc.identifier.scopuseid_2-s2.0-34248356290en_HK
dc.identifier.hkuros134884en_HK
dc.identifier.hkuros152628-
dc.identifier.hkuros137465-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34248356290&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume37en_HK
dc.identifier.issue8en_HK
dc.identifier.spage1150en_HK
dc.identifier.epage1157en_HK
dc.identifier.isiWOS:000248526000006-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridMak, JCW=7103323094en_HK
dc.identifier.scopusauthoridHo, SP=12794365900en_HK
dc.identifier.scopusauthoridLeung, HCM=34968372500en_HK
dc.identifier.scopusauthoridCheung, AHK=12795914100en_HK
dc.identifier.scopusauthoridLaw, BKW=36639650600en_HK
dc.identifier.scopusauthoridSo, LKY=35985409300en_HK
dc.identifier.scopusauthoridChan, JWM=34967874700en_HK
dc.identifier.scopusauthoridChau, CH=7102320975en_HK
dc.identifier.scopusauthoridLam, WK=7203021937en_HK
dc.identifier.scopusauthoridIp, MSM=7102423259en_HK
dc.identifier.scopusauthoridChanYeung, M=54790582200en_HK
dc.identifier.citeulike1469222-

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