AIR POLLUTION INDUCES OXIDATIVE STRESS IN A GENETICALLY SUSCEPTIBLE POPULATION

Abstract

ISEE-35 Aim: To investigate the effect of genetic polymorphism on oxidative damage by air pollution. Methods: We measured urinary 1-hydroxypyrene (1-OHP) and 8-hydroxydeoxyguanosine (8-OHdG) by HPLC for analysis of exposure and oxidative injury in a study population of university students. After determining the myeloperoxidase (MPO) and manganese superoxide dismutase (MnSOD) polymorphism by PCR and RFLP methods, we studied the genetic modification on the relationship between the urinary level of 1-OHP and 8-OHdG. Results: The median age was 25 years. The subject group consisted of 268 males (93.1%) and 20 females (6.1%). The relation between log 1-OHP and 8-OHdG concentration did not reach statistical significance, without consideration of genetic status (p=0.186). In addition, no significant difference was observed in the level of urinary 8-OHdG by MnSOD and MPO genetic polymorphisms (p=0.533 and p=0.934, respectively). However, we found the significant change of regression coefficient of urinary log 1-OHP level on urinary 8-OHdG concentration by MnSOD and MPO polymorphism, in the multiple regression, controlling for age, sex, BMI, and smoking. In the group with MnSOD Val/Ala or Ala/Ala genotypes, the regression coefficient 3.298 was observed (p=0.046), whereas that for MnSOD Val/Val genotype was 0.380 (p=0.734). A better regression coefficient was obtained in the group with genotypes of MnSOD Val/Ala, Ala/Ala and MPO G/G, together (p=0.041). Conclusion: In the present study, we suggest that oxidative injury by air pollution is modified by the genetic polymorphisms of the enzymes MPO and MnSOD.