Association of Lipid Peroxidation with Antenatal Betamethasone and Oxygen Radical Disorders in Preterm Infants

Abstract

Introduction: Premature infants are highly susceptible to ‘oxygen radical diseases’ (ORD), including bronchopulmonary dysplasia, intraventricular hemorrhage/white matter injury, retinopathy of prematurity, and necrotizing enterocolitis. The incidence of ORD is reduced following antenatal treatment with betamethasone. Oxidant-mediated injury is characterized at the cellular level by peroxidation of lipid membranes. This results in the generation of malondialdehyde (MDA), which can be quantified indirectly by measurement of thiobarbituric acid-reacting substances (TBARS). There is currently no effective way to quantify the risk for ORD. In this study, we analyzed the correlation of early urinary MDA and TBARS with prenatal betamethasone administration and with the development of ORD. Methods: Preterm infants (<30 weeks gestation, n = 25) born at St. Peter’s University Hospital were enrolled. Urine samples were collected during the first 10 days of life and stored at –70°C for 0–21 days. TBARS were quantified by spectrophotometric assay, and malondialdehyde levels measured by HPLC. Subjects were screened for the subsequent development of ORD. Betamethasone administration was defined as one or more doses ≧24 h prior to delivery. Results: Urinary MDA levels increased on days 2–3 and 5–10 relative to day 1 from birth. Maximal urinary MDA concentrations were significantly higher in the ORD group compared to controls, and there was a trend toward increased urinary TBARS in the presence of ORD. Infants receiving prenatal betamethasone demonstrated higher maximal urinary TBARS values during the first 10 days of life than control infants. The length of sample storage from 0 to 3 weeks at –70°C did not significantly affect TBARS measurements. Conclusions: Elevated urinary MDA measurements in the first 10 days are correlated with the risk for ORD. Urinary TBARS concentrations, which are correlated with MDA measurements, can be quantified rapidly and are stable for short-term storage. Our findings suggest that urinary TBARS may be adaptable as a practical tool for assessing the risk for ORD in neonatal intensive care unit patients, allowing clinicians to optimize the use of preventive strategies. Antenatal betamethasone is associated with increased urinary TBARS in the first 10 days of life, indicating that the protective effects of corticosteroids are not mediated through reductions in oxidant-mediated lipid peroxidation.

Protective effect of L-carnitine in a rat model of retinopathy of prematurity

“…Cell membrane oxidation due to ROS results in products of lipid peroxidation such as MDA (18,19). The present study found high levels of MDA in rats with ROP compared to those without ROP, as in previous research (19,20).…”

Urinary Malondialdehyde Levels in Newborns following Delivery Room Resuscitation

“…0.02) between plasma MDA and urinary MDA 24 h later. Studies have reported higher urinary or plasma MDA levels in preterm infants reflecting higher oxidative stress in this population [7][8][9] . Mocatta et al [10] reported higher serum MDA levels in preterm infants compared to term infants, but this study did not estimate urinary MDA concentrations.…”

Evaluation of neonatal jaundice in the Makkah region

“…It has been reported that bilirubin can function as a scavenger of reactive oxygen species9. Malondialdehyde (MDA) is a reactive metabolic product that results from the effects of reactive oxygen species on tissues and from a series of reactions that occur during lipid peroxidation10. Plasma MDA levels are a sensitive indicator of lipid peroxidation and thus of oxidative stress1112.…”