Smoking, genetic polymorphisms of glutathione S-transferases and biological indices of inflammation and cellular adhesion in the STANISLAS study
dc.contributor.author | Bolt, Hermann M. | de |
dc.contributor.author | Habdous, Mohammed | de |
dc.contributor.author | Haddy, Nadia | de |
dc.contributor.author | Herbeth, Bernard | de |
dc.contributor.author | Lambert, Daniel | de |
dc.contributor.author | Ponthieux, Anne | de |
dc.contributor.author | Siest, GĂ©rard | de |
dc.contributor.author | Thier, Ricarda | de |
dc.contributor.author | Visvikis, Sophie | de |
dc.date.accessioned | 2008-06-17T13:46:21Z | |
dc.date.available | 2008-06-17T13:46:21Z | |
dc.date.issued | 2004-09-13 | de |
dc.description.abstract | A recent clinical study has focused on: 1- the interaction between genetic variants of glutathione S-transferases M1 and T1 (GSTM1 and GSTT1) and smoking on the risk of cardiovascular diseases, 2- the potential capacity of GSTM1 and T1 genotypes in modifying the effect of smoking on inflammation and endothelial function. In this study, we investigated whether carriage of these 2 polymorphisms altered the smoking impact on biological indices of inflammation and cellular adhesion. White blood cell count (WBC), albumin, C-reactive protein (CRP), interleukine-6 (IL-6), tumor necrosis factor-alpha (TNF-a), L-selectin, E-selectin, P-selectin and intracellular adhesion molecule-1 (ICAM-1) were measured in 189 non-smokers and 76 smokers (aged 20-55 years) genotyped for the GSTM1 and T1 polymorphisms. Accounting for age and sex, smokers lacking GSTM1 had a higher WBC count, CRP and ICAM-1 levels as compared to the other groups; interaction term between smoking and genotype being significant (p=0.05). Conversely, non-smokers lacking GSTM1 had a higher levels of TNF-a; the test for interaction being significant (p=0.05). No significant interaction was found between smoking and GSTT1 genotypes, considering the 9 biological indices. However, significantly lower levels of IL-6 were noticed for non-smokers with GSTT1-0 null allele (p=0.05). Our study confirms previous results showing that GSTM1 polymorphism could modulate the interrelationships between smoking and biological markers of inflammation and endothelial function. | en |
dc.identifier.issn | 1611-2156 | de |
dc.identifier.uri | http://hdl.handle.net/2003/25637 | |
dc.identifier.uri | http://dx.doi.org/10.17877/DE290R-8172 | |
dc.language.iso | en | de |
dc.relation.ispartofseries | EXCLI Journal ; Vol. 3, 2004 | en |
dc.subject | adhesion | en |
dc.subject | glutathione S-transferase polymorphism | en |
dc.subject | inflammation | en |
dc.subject | molecule | en |
dc.subject | smoking | en |
dc.subject.ddc | 610 | |
dc.title | Smoking, genetic polymorphisms of glutathione S-transferases and biological indices of inflammation and cellular adhesion in the STANISLAS study | en |
dc.type | Text | de |
dc.type.publicationtype | article | de |
dcterms.accessRights | open access | |
eldorado.dnb.zdberstkatid | 2132560-1 |
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