Dynamic Thiol-Disulfide Homeostasis in Lung Transplant Recipients

<bold>Objectives: </bold>In this study, we investigated dynamic thiol-disulfide homeostasis as a new indicator of oxidative stress in lung transplant recipients. In addition, we compared dynamic thiol-disulfide homeostasis parameters according to transplant indication and time after transplant.<bold>Materials and methods: </bold>This study had a single-center, observational, randomized design. In terms of transplant indications, lung transplant recipients were grouped as chronic obstructive pulmonary disease, interstitial lung disease, bronchiectasis, and other indications. To make comparisons based on time after transplant, lung transplant recipients were categorized into the following groups: >6 and <= 24 months, >24 and <= 48 months, >48 and <= 72 months, and >72 months. A fully automated spectrophotometric technique was used to measure dynamic thiol-disulfide homeostasis in fasting blood samples.<bold>Results: </bold>Our study included 34 lung transplant recipients and 36 healthy volunteers. Native thiol (P = .005) and total thiol levels (P = .06) were lower in lung transplant recipients. Disulfide levels were similar. Disulfide-to-native thiol (P = .027) and disulfide-to-total thiol ratios (P = .027) were significantly higher in lung transplant recipients. Native thiol-to-total thiol ratios were lower in lung transplant recipients (P = .027). When we examined patients according to transplant indication, no statistically significant differences were found in dynamic thiol-disulfide homeostasis parameters, except for total thiol and disulfide levels. We also found no significant differences when we examined dynamic thiol-disulfide homeostasis parameters according to time after transplant.<bold>Conclusions: </bold>Thiol-related antioxidant activity is significantly reduced after lung transplant, regardless of indication and transplant time. Ensuring oxidative balance in lung transplant recipients with an antioxidant supplement regimen can prevent damage from oxidative stress.