Association Between GSTT1 and GSTM1 Gene Deletions and Oxidative Stress Markers in a Local Population

Background Glutathione S Transferase Mu 1 (GSTM1) and Theta 1 (GSTT1) gene deletions lead to total loss of enzyme activity, which may explain an inability to detoxify reactive electrophiles and increased oxidative stress susceptibility. Although associations between redox biomarkers have been studied worldwide, there is no data yet on Iraqi populations, of whom 20 million are living in areas of high environmental exposure to pro-oxidant pollutants, such as occurs in Babil Province. Materials and Methods A cross-sectional study of 267 adults from Babil, Iraq. Multiplex PCR with internal controls by β-globin for GSTM1 and GSTT1 genotypes. We quantified serum oxidative stress biomarkers malondialdehyde (MDA, TBARS validated by HPLC), total antioxidant capacity (TAC, measured by FRAP), and 8-hydroxy-2′-deoxyguanosine (8-OHdG, ELISA). Multivariable linear regression adjusted for age, sex, BMI, smoking and occupational exposure. Results The GSTM1 null frequency was 59.5%, GSTT1 null 28.1%, and the double-null (GSTM1⁻/GSTT1⁻) 15.7%. Independent of covariates, double-null individuals had significantly raised MDA (+ 57.9%, p < 0.001) and 8-OHdG (+ 66.1%, p < 0.001), and significantly lowered TAC (–22.7%, p < 0.001) vs wild-type. We found a statistically significant interaction between double-null genotype and occupational exposure (pinteraction = 0.018–0.034), strongly supporting that oxidative damage is enhanced when people with a double-null genotype are in high-exposure environments. Conclusion The double-null genotype of abundant homozygous deletions in GSTM1 and GSTT1 is significantly associated with systemic oxidative stress in this Iraqi cohort, where the effects are aggravated with particular environmental exposures. Conclusion This study demonstrates the importance of genotype-informed public health approaches in high-risk occupational groups and providing initial pharmacogenomic data for Iraq.