title: Association between inflammatory marker, environmental lead exposure, and glutathione S-transferase gene.
abstract: A number of studies suggested that lead is related to the induction of oxidative stress, and alteration of immune response. In addition, modifying these toxic effects varied partly by GST polymorphism. The objectives of this study were to assess the association between the lead-induced alteration in serum hs-CRP, with GSTM1, GSTT1, and GSTP1 Val105Ile genetic variations and the health consequence from environmental lead exposure. The 924 blood samples were analyzed for blood lead, CRP, and genotyping of three genes with real-time PCR. Means of blood lead and serum hs-CRP were 5.45 μ g/dL and 2.07 mg/L. Both CRP and systolic blood pressure levels were significantly higher for individuals with blood lead in quartile 4 (6.48-24.63 μ g/dL) compared with those in quartile 1 (1.23-3.47 μ g/dL, P < 0.01). In particular, in men with blood lead >6.47 μ g/dL the adjusted odds ratio (OR) of CRP levels for individuals with GSTP1 variants allele, GSTM1 null, GSTT1 null, double-null GSTM1, and GSTT1 compared with wild-type allele was 1.46 (95% CI; 1.05-2.20), 1.32 (95% CI; 1.03-1.69), 1.65 (95% CI; 1.17-2.35), and 1.98 (95% CI; 1.47-2.55), respectively. Our findings suggested that lead exposure is associated with adverse changes in inflammatory marker and SBP. GST polymorphisms are among the genetic determinants related to lead-induced inflammatory response.
authors.affiliation: Department of Medicine, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Bangkok 10400, Thailand. jintana.sir@mahidol.ac.th
authors.forename: Jintana
authors.initials: J
authors.lastname: Sirivarasai
authors.forename: Winai
authors.initials: W
authors.lastname: Wananukul
authors.forename: Sming
authors.initials: S
authors.lastname: Kaojarern
authors.forename: Suwannee
authors.initials: S
authors.lastname: Chanprasertyothin
authors.forename: Nisakron
authors.initials: N
authors.lastname: Thongmung
authors.forename: Wipa
authors.initials: W
authors.lastname: Ratanachaiwong
authors.forename: Thanyachai
authors.initials: T
authors.lastname: Sura
authors.forename: Piyamit
authors.initials: P
authors.lastname: Sritara
mesh_terms: D000328:Adult; D000483:Alleles; D019943:Amino Acid Substitution; D015415:Biomarkers / Q000097:blood; D001794:Blood Pressure / Q000187:drug effects / Q000235:genetics; D002097:C-Reactive Protein / Q000235:genetics / Q000378:metabolism; D004781:Environmental Exposure / Q000009:adverse effects*; D051549:Glutathione S-Transferase pi / Q000097:blood / Q000235:genetics*; D005982:Glutathione Transferase / Q000097:blood / Q000235:genetics*; D006801:Humans; D007854:Lead / Q000493:pharmacokinetics*; D007855:Lead Poisoning / Q000097:blood / Q000201:enzymology / Q000235:genetics; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress / Q000187:drug effects / Q000235:genetics; D011110:Polymorphism, Genetic
chemical_list: D015415:Biomarkers; D002097:C-Reactive Protein; D051549:Glutathione S-Transferase pi; D005982:Glutathione Transferase; D007854:Lead; C413545:glutathione S-transferase T1; C496556:GSTP1 protein, human