J Korean Med Sci.  2006 Dec;21(6):1021-1027. 10.3346/jkms.2006.21.6.1021.

GSTM1 and GSTP1 Polymorphisms as Potential Factors for Modifying the Effect of Smoking on Inflammatory Response

Affiliations
  • 1Department of Preventive Medicine, Seoul National University College of Medicine, 28 Yongon-dong, Chongno-gu, Seoul, Korea. ychong1@snu.ac.kr
  • 2Department of Occupational and Environmental Medicine, Inha University Hospital, Incheon, Korea.
  • 3Department of Family Medicine, Inha University Hospital, Incheon, Korea.
  • 4Department of Preventive Medicine, Ewha Womans University College of Medicine, Seoul, Korea.
  • 5Center for Cancer Prevention and Detection, National Cancer Center Hospital, Goyang, Korea.
  • 6Institute of Environmental Medicine, SNUMRC, Seoul, Korea.

Abstract

Inflammation has been known to be an important underlying condition for development of various diseases including cancer. The aims of this study were to investigate whether tobacco smoke exposure increases the level of inflammation biomarkers and the GSTM1 and GSTP1 gene polymorphisms are associated with inflam matory response due to tobacco smoke exposure. We measured urinary cotinine level in 300 healthy university students. Total serum TNF-alpha levels and blood WBC counts were determined to evaluate inflammatory response. Allelic loss of the GSTM1 and the GSTP1 (Ile105Val) polymorphism were determined by PCR and RFLP. Tobacco smoke exposure was found to be associated with increase of both TNF-alpha level and WBC count. Particularly, smokers with combination of GSTM1 null and GSTP1 AG or GG genotypes showed higher TNF-alpha level than those with the other genotype combinations (p=0.07). This result suggests that smoking may induce inflammation measured as TNF-alpha level or WBC count and combinations of the GSTM1 and GSTP1 polymorphisms may modify the effect of smoking on serum TNF-alpha level.

Keyword

Smoking; Inflammation; Tumor Necrosis Factor-alpha; Leukocytes; glutathione S-transferase M1; Glutathione S-Transferase pi; Polymorphism, Genetic

MeSH Terms

Tumor Necrosis Factor-alpha/blood
Students
Smoking/*epidemiology/*genetics/immunology
Risk Factors
Risk Assessment/*methods
Prevalence
Polymorphism, Single Nucleotide/genetics
Male
Korea/epidemiology
Inflammation/*epidemiology/*genetics/immunology
Humans
Glutathione Transferase/*genetics
Glutathione S-Transferase pi/*genetics
Genetic Predisposition to Disease/epidemiology/genetics
Female
Adult

Figure

  • Fig. 1 Serum TNF-α levels according to combinations of GSTM1 and GSTP1 polymorphisms in strata divided by pack year (A) or urinary cotinine level (B). M1, GSTM1 present; M1*, GSTM1 null; P1: GSTP1 AA; P1*, GSTP1 AG or GG. ANOVA was used to compare the means of TNF-α levels according to genotype combinations in strata divided by pack year (pack year=0, p=0.40; and pack year >0, p=0.07, respectively) or cotinine level (cotinine=0, p=0.41; and cotinine >0, p=0.15, respectively). The number in each bar indicates number of subjects included in strata of each genotype combination in smoker and nonsmoker.

  • Fig. 2 Blood WBC counts according to combinations of GSTM1 and GSTP1 polymorphisms in strata divided by pack year (A) or urinary cotinine level (B). M1, GSTM1 present; M1*, GSTM1 null; P1: GSTP1 AA; P1*, GSTP1 AG or GG. ANOVA was used to compare the means of WBC counts according to genotype combinations in strata divided by pack year (pack year=0, p=0.77; and pack year >0, p=0.34, respectively) or cotinine level (cotinine=0, p=0.95; and cotinine >0, p=0.15, respectively). The number in each bar indicates number of subjects included in strata of each genotype combination in smoker and nonsmoker.


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