Abstract
BackgroundNeonatal intermittent hypoxia (IH) results in oxidative distress in preterm infants with immature antioxidant systems, contributing to lung injury. Coenzyme Q10 (CoQ10) and fish oil protect against oxidative injury. We tested the hypothesis that CoQ10 is more effective than fish oil for prevention of IH-induced lung injury in neonatal rats.MethodsNewborn rats were exposed to two clinically relevant IH paradigms at birth (P0): (1) 50% O2 with brief hypoxia (12% O2); or (2) room air (RA) with brief hypoxia (12% O2), until P14 during which they were supplemented with daily oral CoQ10, fish oil, or olive oil from P0 to P14. Pups were studied at P14 or placed in RA until P21 with no further treatment. Lungs were assessed for histopathology and morphometry; biomarkers of oxidative stress and lipid peroxidation; and antioxidants.ResultsOf the two neonatal IH paradigms 21%/12% O2 IH resulted in the most severe outcomes, evidenced by histopathology and morphometry. CoQ10 was effective for preserving lung architecture and reduction of IH-induced oxidative stress biomarkers. In contrast, fish oil resulted in significant adverse outcomes including oversimplified alveoli, hemorrhage, reduced secondary crest formation and thickened septae. This was associated with elevated oxidants and antioxidants activities.ConclusionsData suggest that higher FiO2 may be needed between IH episodes to curtail the damaging effects of IH, and to provide the lungs with necessary respite. The negative outcomes with fish oil supplementation suggest oxidative stress-induced lipid peroxidation.
Highlights
Low gestational age neonates (ELGANs), born at < 28 weeks gestation often receive supplemental oxygen for respiratory support, with or without mechanicalD’Agrosa et al Respir Res (2021) 22:196 than dispersed intermittent hypoxia (IH) events in neonatal rats [3]
Weights Overall, exposure to both IH paradigms resulted in lower percentage change in body weight at P14 (50/12% O 2: 225.5 ± 7.1%, p < 0.01; 21/12% O2: 191.8 ± 9.4%, p < 0.01) and remained suppressed during the recovery/reoxygenation period at P21 (50/12% O2: 319.9 ± 12.3%, p < 0.01; 21/12% O2: 327.2 ± 12.1%, p < 0.01) compared to room air (RA) at P14 (328.1 ± 7.5%) and P21 (513.0 ± 13.5%)
The major findings of this report are: (1) while both neonatal IH paradigms were damaging to the immature lungs, resolution with normoxia between IH episodes was more injurious than IH resolving in hyperoxia
Summary
Low gestational age neonates (ELGANs), born at < 28 weeks gestation often receive supplemental oxygen for respiratory support, with or without mechanicalD’Agrosa et al Respir Res (2021) 22:196 than dispersed IH events in neonatal rats [3]. Exposure of immature lungs to supraphysiological oxygen, combined with surfactant deficiency and poor nutrition result in poor alveolar development and microvascular maturation. Recent studies show that oxygen toxicity/hyperoxia and oxidative stress plays a significant role in the development of BPD/CLD [9]. ELGANS are deficient in antioxidants which generally increase with advancing gestation, rendering them susceptible to oxidative stress and related diseases [10, 11]. Neonatal intermittent hypoxia (IH) results in oxidative distress in preterm infants with immature antioxidant systems, contributing to lung injury. Coenzyme Q10 (CoQ10) and fish oil protect against oxidative injury. We tested the hypothesis that CoQ10 is more effective than fish oil for prevention of IH-induced lung injury in neonatal rats
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