Association of lipid peroxidation with antenatal betamethasone and oxygen radical disorders in preterm infants

Barry Weinberger, Mujahid Anwar, Samir Henien, Ana Sosnovsky, Mark Hiatt, Nina Jochnowitz, Gisela Witz, Thomas Hegyi

Research output: Contribution to journalArticle

24 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)121-127
Number of pages7
JournalBiology of the Neonate
Volume85
Issue number2
DOIs
StatePublished - Apr 16 2004

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Betamethasone
Premature Infants
Lipid Peroxidation
Reactive Oxygen Species
Malondialdehyde
Oxidants
thiobarbituric acid
Bronchopulmonary Dysplasia
Retinopathy of Prematurity
Necrotizing Enterocolitis
Neonatal Intensive Care Units
Wounds and Injuries
Membrane Lipids
Adrenal Cortex Hormones
High Pressure Liquid Chromatography
Urine
Parturition
Hemorrhage
Pregnancy

All Science Journal Classification (ASJC) codes

  • Pediatrics, Perinatology, and Child Health
  • Developmental Biology

Keywords

  • Betamethasone
  • Malondialdehyde
  • Oxidant injury
  • Oxygen
  • Premature infant

Cite this

Weinberger, Barry ; Anwar, Mujahid ; Henien, Samir ; Sosnovsky, Ana ; Hiatt, Mark ; Jochnowitz, Nina ; Witz, Gisela ; Hegyi, Thomas. / Association of lipid peroxidation with antenatal betamethasone and oxygen radical disorders in preterm infants. In: Biology of the Neonate. 2004 ; Vol. 85, No. 2. pp. 121-127.
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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.",
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Weinberger, B, Anwar, M, Henien, S, Sosnovsky, A, Hiatt, M, Jochnowitz, N, Witz, G & Hegyi, T 2004, 'Association of lipid peroxidation with antenatal betamethasone and oxygen radical disorders in preterm infants', Biology of the Neonate, vol. 85, no. 2, pp. 121-127. https://doi.org/10.1159/000074968

Association of lipid peroxidation with antenatal betamethasone and oxygen radical disorders in preterm infants. / Weinberger, Barry; Anwar, Mujahid; Henien, Samir; Sosnovsky, Ana; Hiatt, Mark; Jochnowitz, Nina; Witz, Gisela; Hegyi, Thomas.

In: Biology of the Neonate, Vol. 85, No. 2, 16.04.2004, p. 121-127.

Research output: Contribution to journalArticle

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T1 - Association of lipid peroxidation with antenatal betamethasone and oxygen radical disorders in preterm infants

AU - Weinberger, Barry

AU - Anwar, Mujahid

AU - Henien, Samir

AU - Sosnovsky, Ana

AU - Hiatt, Mark

AU - Jochnowitz, Nina

AU - Witz, Gisela

AU - Hegyi, Thomas

PY - 2004/4/16

Y1 - 2004/4/16

N2 - 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.

AB - 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.

KW - Betamethasone

KW - Malondialdehyde

KW - Oxidant injury

KW - Oxygen

KW - Premature infant

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