Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2003-12-3
pubmed:abstractText
Recent epidemiologic studies suggest that polymorphisms of glutathione-S-transferases M1 and T1 (GSTM1/GSTT1) modify the effects of cigarette smoking on risk of coronary heart disease (CHD). Since GSTs are able to detoxify numerous toxic compounds and products of oxidative stress, it is possible that GST genotypes may also modify the capacity of smoking to invoke a chronic inflammatory response. A cross-sectional analysis, using a subset of participants (n = 989) in a large (n = 15, 792) biracial cohort, was used to evaluate levels of nine markers of inflammation, hemostasis, and endothelial function by different combinations of GST genotypes and cigarette smoking status. Participants with the GSTM1 null (GSTM1-0) genotype and > or = 20 pack-years of smoking had the highest mean levels of CRP, fibrinogen, von Willebrand factor, ICAM-1, and VCAM-1 and lowest mean levels of albumin compared to other combinations of genotype and smoking. However, a formal test for interaction between GSTM1 genotype and smoking was statistically significant only for albumin. By contrast, participants who had the functional GSTT1 genotype (GSTT1-1) and smoked > or = 20 pack-years had the highest mean levels of only CRP and fibrinogen. The results of this study provide some limited evidence that GSTM1 and GSTT1 polymorphisms modify the effect of smoking on inflammation, hemostasis, and endothelial function.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0021-9150
pubmed:author
pubmed:copyrightInfo
Copyright 2003 Elsevier Ireland Ltd.
pubmed:issnType
Print
pubmed:volume
171
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
265-72
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:14644396-Cohort Studies, pubmed-meshheading:14644396-Comorbidity, pubmed-meshheading:14644396-Coronary Artery Disease, pubmed-meshheading:14644396-Cross-Sectional Studies, pubmed-meshheading:14644396-Endothelium, Vascular, pubmed-meshheading:14644396-Female, pubmed-meshheading:14644396-Genetic Markers, pubmed-meshheading:14644396-Genetic Predisposition to Disease, pubmed-meshheading:14644396-Glutathione Transferase, pubmed-meshheading:14644396-Hemostasis, pubmed-meshheading:14644396-Humans, pubmed-meshheading:14644396-Incidence, pubmed-meshheading:14644396-Inflammation Mediators, pubmed-meshheading:14644396-Linear Models, pubmed-meshheading:14644396-Male, pubmed-meshheading:14644396-Middle Aged, pubmed-meshheading:14644396-Multivariate Analysis, pubmed-meshheading:14644396-Polymorphism, Genetic, pubmed-meshheading:14644396-Probability, pubmed-meshheading:14644396-Prognosis, pubmed-meshheading:14644396-Residence Characteristics, pubmed-meshheading:14644396-Risk Factors, pubmed-meshheading:14644396-Sensitivity and Specificity, pubmed-meshheading:14644396-Severity of Illness Index, pubmed-meshheading:14644396-Smoking, pubmed-meshheading:14644396-United States
pubmed:year
2003
pubmed:articleTitle
Glutathione-S-transferase genotypes, smoking, and their association with markers of inflammation, hemostasis, and endothelial function: the atherosclerosis risk in communities (ARIC) study.
pubmed:affiliation
Department of Epidemiology, University of North Carolina, Chapel Hill, NC, USA.
pubmed:publicationType
Journal Article, Comparative Study