title: Influence of genetic polymorphisms in oxidative stress related genes and smoking on plasma MDA-LDL, soluble CD40 ligand, E-selectin and soluble ICAM1 levels in patients with coronary artery disease.
abstract: BACKGROUND
  Previous studies have shown that oxidative stress plays an important role in coronary heart disease. Polymorphisms in key enzymes that regulate oxidative stress may play a role in atherogenicity and were investigated in this study.
  
  
  METHODS
  One hundred and forty-three patients with angiographically proven coronary artery disease were studied. The effect of the C242T polymorphism of the p22phox gene, an essential component of the NADH/NADPH oxidase, and glutathione-S-transferase T1, M1 and P1 polymorphisms on plasma MDA-LDL, soluble CD40 ligand, E-selectin and soluble ICAM1 levels was determined. Genotyping of the p22 phox C242T polymorphism was performed by RFLP analysis, and GSTT1, GSTM1 and GSTP1 genotypes were determined using a multiplex PCR assay. The MDA-LDL, sCD40L, E-selectin and sICAM1 levels were determined using ELISA.
  
  
  RESULTS
  Patients with the TT or TC genotype of the p22 phox C242T polymorphism had significantly higher plasma MDA-LDL levels compared to those of the CC genotype. Plasma E-selectin and soluble ICAM1 levels were significantly higher in the TT or TC genotype compared to that of the CC genotype. In GSTT1+ patients, plasma MDA-LDL levels were significantly higher than those of GSTT1- patients.
  
  
  CONCLUSIONS
  Genetic polymorphism of the p22 phox gene had a significant effect on plasma lipid peroxidation and endothelial function through oxidative stress. The results of this study confirm the effect of NADH/NADPH oxidase on atherogenecity.
authors: Department of Medicine, Division of Nephrology, Hypertension and Endocrinology, Nihon University School of Medicine, Tokyo, Japan. tueno@med.nihon-u.ac.jp
authors: Takahiro
authors: T
authors: Ueno
authors: Hideyuki
authors: H
authors: Watanabe
authors: Noboru
authors: N
authors: Fukuda
authors: Akiko
authors: A
authors: Tsunemi
authors: Kazunobu
authors: K
authors: Tahira
authors: Taro
authors: T
authors: Matsumoto
authors: Tadateru
authors: T
authors: Takayama
authors: Masaaki
authors: M
authors: Chiku
authors: Satoshi
authors: S
authors: Saito
authors: Yuichi
authors: Y
authors: Sato
authors: Atsushi
authors: A
authors: Hirayama
authors: Koichi
authors: K
authors: Matsumoto
authors: Masayoshi
authors: M
authors: Soma
mesh_terms: D000368:Aged; D023201:CD40 Ligand / Q000097:blood*; D003327:Coronary Disease / Q000097:blood / Q000201:enzymology / Q000235:genetics*; D019040:E-Selectin / Q000097:blood; D051549:Glutathione S-Transferase pi / Q000235:genetics; D005982:Glutathione Transferase / Q000235:genetics; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood*; D008077:Lipoproteins, LDL / Q000097:blood; D008315:Malondialdehyde / Q000097:blood*; D008875:Middle Aged; D019255:NADPH Oxidases / Q000235:genetics; D018384:Oxidative Stress / Q000235:genetics*; D011110:Polymorphism, Genetic; D012907:Smoking / Q000097:blood* / Q000235:genetics; D012995:Solubility
chemical_list: D023201:CD40 Ligand; D019040:E-Selectin; D051549:Glutathione S-Transferase pi; D005982:Glutathione Transferase; D018799:Intercellular Adhesion Molecule-1; D008077:Lipoproteins, LDL; D008315:Malondialdehyde; D019255:NADPH Oxidases; C086986:CYBA protein, human; C413545:glutathione S-transferase T1