The Leucocyte Telomere Length, and Null Genotypes and the Risk of Chronic Obstructive Pulmonary Disease.

Chronic obstructive pulmonary disease (COPD) is characterized by chronic inflammation and oxidative stress both in the airways and blood and other organs. Elevated oxidative stress and inflammation have been reported to affect leucocyte telomere length (LTL). Glutathione S-transferase (GST) enzymes are a large family of xenobiotic-metabolizing enzymes that utilize different ROS products. We aimed to explore the link between and gene polymorphisms, LTL and COPD risk. For , we genotyped 152 COPD patients and 131 non-affected controls; for , we genotyped 149 COPD patients and 130 controls. We were able to assess TL for 91 patients and 88 controls. There was a significant difference in the null genotype frequency between the patients and controls (0.59 vs. 0.38, ≤ 0.000), but such was not found for ( = 0.192). When combining both polymorphisms, we obtained a significantly greater presence of at least one null genotype among patients (0.12 vs. 0.05, = 0.027). An association between and LTL was not found. COPD patients carrying the null genotype had shorter telomeres compared to those carrying the non-null genotype (15,720 bp vs. 22,442 bp, = 0.008); as for the controls, it was the opposite (31,354 bp vs. 17,800 bp, = 0.020). The significance in both groups remained when combining and (COPD (at least one null) 16,409 bp vs. COPD (non-null) 22,092 bp, = 0.029; control (at least one null) 29,666 bp vs. control (non-null) 16,370 bp, = 0.027). The total glutathione level in non-null controls was higher compared to the null genotype (15.39 ng/mL vs. 5.53 ng/mL, = 0.002). In COPD patients, we found no association ( = 0.301). In conclusion, according to our results, , but not 1, null genotypes might play a role in leucocyte telomere shortening, and thus be involved in the pathogenesis of COPD.