IMR Press / FBE / Volume 2 / Issue 1 / DOI: 10.2741/E96

Frontiers in Bioscience-Elite (FBE) is published by IMR Press from Volume 13 Issue 2 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article
Mitochondrial DNA damage analysis in bronchoalveolar lavage cells of preterm infants
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1 Department of Pediatrics Maastricht University Medical Center (MUMC+), GROW School for Oncology and Developmental Biology, 6202 AZ Maastricht, The Netherlands
2 Department of Clinical Genetics, Maastricht University Medical Center (MUMC+), GROW School for Oncology and Developmental Biology, 6202 AZ Maastricht, The Netherlands
3 Department of Neonatology, University Hospital Gasthuisberg, 3000 Leuven, Belgium

*Author to whom correspondence should be addressed.

Academic Editor: Giovanni Li Volti

Front. Biosci. (Elite Ed) 2010, 2(1), 361–368; https://doi.org/10.2741/E96
Published: 1 January 2010
(This article belongs to the Special Issue Biochemical markers in biological fluids)
Abstract

In mechanically ventilated preterm infants, the combination of immaturity, volutrauma, oxidative stress, and inflammatory processes can lead to chronic lung injury. Mitochondrial DNA (mtDNA) is more susceptible to oxidative damage than nuclear DNA. We aimed to investigate the level of mtDNA damage (deletions, mutations and changes in copy number) in bronchoalveolar lavage (BAL) cells from 10 preterm infants (27-30 weeks). A first BAL (BAL1) was done within 24 h of endotracheal intubation and BAL2 was performed 30-103 h thereafter. Deletions were analyzed by long range PCR, point mutations by heteroduplex analysis of the D-loop region, and copy number changes by real-time PCR. Using these methods, no deletions were found in any of the BAL samples. When BAL1 and BAL2 samples were compared no new mutations were found. In contrast, a marked decrease in mtDNA copy number was observed in 5 patients. In conclusion, we found that exposure of preterm infants to short term mechanical ventilation did not lead to detrimental consequences for the mtDNA in the form of mutations or deletions.

Keywords
Prematurity
Mechanical ventilation
Oxidant stress
Lung injury
Mitochondrial DNA
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