Abstract
Oxidative stress may play a central role in the onset of many diseases during the neonatal period. Malondialdehyde (MDA) is a marker of lipid peroxidation. The aim of this study was to evaluate a new marker, the malondialdehyde adduct to hemoglobin (MDA-Hb), which is measured in red blood cells (RBCs) and thus does not require that an additional blood sample be drawn. In this prospective study, we first adapted the measurement method previously described to Hb solutions obtained from washed RBCs and then evaluated the suitability of the method for use in neonates. MDA-Hb concentrations were measured by liquid chromatography-mass spectrometry. We compared the concentrations of MDA-Hb between preterm and term neonates. Erythrocyte samples were collected at birth from 60 healthy neonates (29 full-term and 31 preterm), as well as from 50 preterm neonates with uncomplicated postnatal evolution during the first months of life. We found a significantly higher MDA-Hb concentration at birth in preterm neonates (P = 0.002). During the first months of life, MDA-Hb concentrations were 9.4 nanomol/g Hb in hospitalized preterm neonates. MDA-Hb could be used to assess oxidative stress in preterm neonates. Together with clinical variables, it could be a useful marker for oxidative stress exposition in these higher risk patients.
Highlights
Growing evidence indicates that an imbalance between oxidative stress (OS) and antioxidant defense mechanisms plays an important role in the onset of many diseases during the neonatal period [1, 2]
These changes and processes greatly increase the production of free radicals, which must be controlled by the antioxidant defense system that has been maturing over the course of gestation [5, 6]
Free radicals are too short-lived to be detected directly in clinical systems, but oxygen free radicals react with lipids to produce lipid peroxidation products, which when measured serve as indirect biomarkers of in vivo oxidative stress status and related diseases
Summary
Growing evidence indicates that an imbalance between oxidative stress (OS) and antioxidant defense mechanisms plays an important role in the onset of many diseases during the neonatal period [1, 2]. Birth is associated with a strong OS related to the rapid change from a relatively hypoxic intrauterine environment to the extrauterine environment (5-fold increase in alveolar PO2) and several physiologic processes involved in the delivery [3, 4] These changes and processes greatly increase the production of free radicals, which must be controlled by the antioxidant defense system that has been maturing over the course of gestation [5, 6]. Free radicals are too short-lived to be detected directly in clinical systems, but oxygen free radicals react with lipids to produce lipid peroxidation products, which when measured serve as indirect biomarkers of in vivo oxidative stress status and related diseases Among these products, malondialdehyde (MDA) is one of the principal and most studied lowmolecular-weight end products. It is highly cytotoxic because of its ability to bind proteins or nucleic acids very quickly [7]
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