Objective: Reactive oxygen species (ROS) contribute to oxidative lung injury. The glutathione-S-transferases (GST) family and microsomal epoxide hydrolase (mEPHx) enzymes detoxify ROS, and genetic polymorphisms alter this detoxification. We hypothesized that polymorphisms encoding for less efficient enzymes were associated with bronchopulmonary dysphasia (BPD).
Study design: We determined allelic distribution of these polymorphisms in a pilot study of 35 BPD cases and 98 controls. chi2 and regression analysis were performed.
Results: GST P1 val105ile distribution differed between the groups, with the more efficient val/val allele predominantly in controls (p< or =0.05). When controlling for race and sex, BPD cases were less likely to be homozygotes for the val/val isoform (OR 0.21, CI: 0.045-0.95, p=0.04) and more likely to possess the less efficient ile isoform (OR 4.5, CI: 1.0-20.7, p=0.05).
Conclusions: This pilot study suggests that BPD is associated with the presence of the GST-P1 105ile allele. Future prospective studies are warranted.