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Cord Blood Adductomics Reveals Oxidative Stress Exposure Pathways of Bronchopulmonary Dysplasia
Erika T Lin1, Yeunook Bae2, Robert Birkett3
1Department of Pediatrics, Division of Neonatology, University of California San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.
Insights
Oxidative stress (OS) adducts in infant blood are linked to bronchopulmonary dysplasia (BPD). This study used adductomics to identify OS biomarkers, potentially guiding antioxidant strategies for infant health.
Area of Science:
- Environmental Health
- Biomarker Discovery
- Neonatal Medicine
Background:
- Perinatal oxidative stress (OS) is a significant factor in bronchopulmonary dysplasia (BPD) development.
- Adductomics, an exposure science method, quantifies protein adducts to assess OS exposure.
- Human serum albumin (HSA) adducts offer a stable measure of OS exposure due to their long half-life.
Purpose of the Study:
- To investigate the association between OS-related adducts and BPD in preterm and full-term infants.
- To characterize the neonatal-perinatal exposome using adductomics.
- To identify novel OS exposure biomarkers for BPD prevention.
Main Methods:
- Targeted and untargeted adductomics analysis of infant plasma (cord blood and postnatal samples).
- Quantification of known and unknown adducts using high-performance liquid chromatography-mass spectrometry (HPLC-MS).
- Study included 205 preterm and 51 full-term infants.
Main Results:
- 105 adducts were identified in infant blood samples.
- 51 known OS adducts were significantly increased in infants with BPD.
- Postnatal OS adduct levels correlated with supplemental oxygen exposure.
Conclusions:
- Adductomics successfully identified OS-related biomarkers associated with BPD.
- This study provides the first investigation into the neonatal-perinatal exposome.
- Findings may inform the development of antioxidant strategies to improve infant respiratory health.
Abstract:
Fetal and neonatal exposures to perinatal oxidative stress (OS) are key mediators of bronchopulmonary dysplasia (BPD). To characterize these exposures, adductomics is an exposure science approach that captures electrophilic addition products (adducts) in blood protein. Adducts are bound to the nucleophilic cysteine loci of human serum albumin (HSA), which has a prolonged half-life. We conducted targeted and untargeted adductomics to test the hypothesis that adducts of OS vary with BPD. We studied 205 preterm infants (≤28 weeks) and 51 full-term infants from an ongoing birth cohort. Infant plasma was collected at birth (cord blood), 1-week, 1-month, and 36-weeks postmenstrual age. HSA was isolated from plasma, trypsin digested, and analyzed using high-performance liquid chromatography-mass spectrometry to quantify previously annotated (known) and unknown adducts. We identified 105 adducts in cord and postnatal blood. A total of 51 known adducts (small thiols, direct oxidation products, and reactive aldehydes) were increased with BPD. Postnatally, serial concentrations of several known OS adducts correlated directly with supplemental oxygen exposure. The application of large-scale adductomics elucidated OS-mediated pathways of BPD. This is the first study to investigate the "neonatal-perinatal exposome" and to identify oxidative stress-related exposure biomarkers that may inform antioxidant strategies to protect the health of future generations of infants.
