Related Experiment Video
Updated: Sep 28, 2026
Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats
Published on: November 20, 2015
Association of lipid peroxidation with hepatocellular injury in preterm infants
Barry Weinberger1, Kazimierz Watorek, Richard Strauss
1University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, New Brunswick, NJ, USA. barryw@pol.net
Insights
Oxidative stress is linked to liver injury in preterm infants receiving total parenteral nutrition (TPN). However, increased urinary thiobarbituric-acid-reacting substances (TBARS), a marker of oxidative stress, did not significantly differ between infants with or without cholestasis.
Area of Science:
- Neonatal Medicine
- Pediatric Gastroenterology
- Biochemistry
Background:
- Cholestasis is a potential complication of total parenteral nutrition (TPN) in preterm infants.
- Oxidative stress, involving reactive oxygen intermediates, is implicated in various neonatal conditions.
- Urinary thiobarbituric-acid-reacting substances (TBARS) serve as a marker for lipid peroxidation and oxidative stress.
Purpose of the Study:
- To investigate the association between TPN-induced cholestasis and increased oxidative stress in preterm neonates.
- To determine if elevated urinary TBARS levels correlate with hepatocellular injury, indicated by serum alanine transaminase (ALT) and aspartate transaminase (AST) levels.
Main Methods:
- A cohort of preterm infants (<35 weeks' gestation) was divided into cholestasis and control groups.
- Urine samples were analyzed for TBARS, and blood samples for serum bilirubin, ALT, AST, and alkaline phosphatase.
- Infants in the cholestasis group had direct bilirubin >2 mg/dl and received TPN for ≥10 days.
Main Results:
- Serum ALT and AST levels were significantly elevated in the cholestasis group compared to controls.
- Urinary TBARS levels showed a correlation with ALT and AST levels across all infants.
- No significant difference in urinary TBARS levels was observed between the cholestasis and control groups.
Conclusions:
- Hepatocellular injury in preterm infants receiving TPN is associated with oxidative stress.
- The degree of cholestasis did not directly correlate with the measured levels of oxidative stress markers (TBARS).
- Further research is needed to elucidate the complex interplay between TPN, cholestasis, and oxidative stress in neonates.
Introduction:
We wished to determine whether cholestasis induced by total parenteral nutrition (TPN) in preterm newborn infants is associated with increased oxidative stress secondary to increased reactive oxygen intermediates. We hypothesized that elevated urinary thiobarbituric-acid-reacting substances (TBARS), a marker of oxidative stress, would be associated with hepatocellular injury as measured by serum alanine transaminase (ALT) and aspartate transaminase (AST) levels.
Materials And Methods:
Preterm infants (<35 weeks' gestation) admitted to the neonatal intensive care unit were enrolled (with their parents' informed consent) in either the 'cholestasis' group (if their direct bilirubin was >2 mg/dl [34.2 micromol/l] and duration of TPN was > or = 10 days [n = 27]) or in the control group. Urine samples for measurement of TBARS (proportionate to lipid peroxidation) and blood specimens for analysis of serum bilirubin, ALT, AST, and alkaline phosphatase were obtained within 24 hours of enrollment.
Results:
The cholestasis and control groups were comparable with respect to gestational age, birth weight, Apgar score, maximum FiO2, and duration of supplemental oxygen administration. Median serum direct bilirubin concentrations in the cholestasis and control groups were, respectively, 3.3 mg/dl (56.4 micromol/l) and 1.7 mg/dl (29.1 micromol/l) (P < 0.001). Serum ALT and AST levels were also elevated in the cholestasis group, but alkaline phosphatase levels did not differ significantly between the groups. Urinary levels of TBARS in all the infants were correlated with ALT and AST but did not differ significantly between cholestatic and control infants.
Discussion:
Our findings suggest that oxidant stress is associated with hepatocellular injury in preterm infants. This effect is not correlated with the degree of cholestasis.
