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Published on: October 19, 2013
Increased heme oxygenase-1 expression in premature infants with respiratory distress syndrome
Ildikó Farkas1, Zoltán Maróti, Márta Katona
1Department of Pediatrics, University of Szeged, Korányi fasor 14-15, Szeged, H-6720, Hungary. ko.farkas@gmail.com
Insights
Preterm infants with respiratory distress syndrome (RDS) show significantly elevated heme oxygenase-1 (HO-1) expression. This increased HO-1, an enzyme protecting against oxidative stress, correlates with disease severity and lower platelet counts.
Area of Science:
- Neonatal medicine
- Biochemistry
- Pathophysiology
Background:
- Oxidative stress is implicated in severe illnesses affecting preterm infants.
- Heme oxygenase-1 (HO-1) is a cytoprotective enzyme against oxygen radical damage.
- Previous studies established HO-1's role in healthy neonates and asymptomatic preterm infants.
Purpose of the Study:
- To investigate heme oxygenase-1 (HO-1) expression in preterm infants diagnosed with respiratory distress syndrome (RDS).
Main Methods:
- Collected blood samples from 28 preterm infants with RDS on days 1, 3, and 5 post-birth.
- Quantified HO-1 mRNA expression using competitive reverse transcriptase PCR.
- Performed quantitative blood counts to assess platelet levels.
Main Results:
- Preterm infants with RDS exhibited an approximate eight-fold increase in HO-1 expression compared to healthy mature and asymptomatic preterm infants.
- A significant negative association was observed between platelet count and HO-1 expression.
- HO-1 induction was notably higher in RDS infants with thrombocytopenia.
Conclusions:
- Respiratory distress syndrome (RDS) in preterm infants is associated with heightened HO-1 expression within the first five days of life.
- Elevated HO-1 expression aligns with the inflammatory and oxidative nature of RDS in neonates.
Abstract:
Oxidative stress is known to play an important role in the pathogenesis of certain severe illnesses in preterm infants. The enzyme heme oxygenase-1 (HO-1) participates in cytoprotection against oxygen radical injury. We have previously described the role of HO-1 in physiologic adaptation by demonstrating the induction of HO-1 in healthy mature neonates and asymptomatic preterm infants. Our current aim was to investigate the HO-1 expression in preterm infants with respiratory distress syndrome (RDS). We collected venous blood samples from 28 preterm infants with RDS on the 1st, 3rd and 5th days after birth. The HO-1 mRNA expression was determined by means of a competitive reverse transcriptase PCR technique, and a quantitative blood count was performed on the residual blood sample. A significant increase in HO-1 expression was found in the preterm infants with RDS as compared with both the healthy mature and the asymptomatic premature groups. The elevation was approximately eight-fold. The platelet count displayed a significant negative association with the HO-1 expression, and in the RDS prematures with thrombocytopenia the HO-1 induction was significantly greater than in those with a normal platelet count. In conclusion, the RDS of prematures is accompanied by an elevated HO-1 expression during the first 5 days of life, consistent with the inflammatory and oxidative characteristics of the disease.
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