Association of glutathione-S-transferase-P1 (GST-P1) polymorphisms with bronchopulmonary dysplasia

Abstract

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 dysplasia (BPD). Study Design: We determined allelic distribution of these polymosphisms in a pilor study of 35 BPD cases and 98 controls. χ2 and regression analysis were performed. Results: GST P1 val105ile distribution differed between the groups, with the more efficient val/val alle predominately in controls (p≤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: The pilot study suggests that BPD is associated with the presence of the GST-P1 105ile alle. Future prospective studies are warranted.