Abstract
Introduction: The role of oxidative stress in bronchopulmonary dysplasia (BPD) pathogenesis has been proved. Taking into account the pathogenic aspects of BPD development, the severity of disease clinical implications can be the result of action of mutant antioxidant enzyme genes, such as manganese superoxide dismutase (MnSOD).
Aims and objectives: The aim of the study is to establish genetic risk factors of BPD development. The objective is to investigate the genetic polymorphism frequency analysis of MnSOD gene at preterm infants with BPD to clarify its contribution to the formation of the disease.
Methods: 20 preterm infants with BPD and 36 premature infants without respiratory disorders have been included in the study. 3 allelic polymorphisms of MnSOD gene have been investigated: replacement of Thymine at position 58 to Cytosine (MnSOD 58 Ile/Thr), replacement of Cytosine at position 60 to Thymine (MnSOD 60 Leu/Phe), replacement of Cytosine at position 16 to Thymine (MnSOD 16 Ala/Val).
Results: The frequency of occurrence of MnSOD 16 Ala/Val mutation in infants with BPD was 90% in comparison with 31.6% in the control group (two-tailed Fisher’s test (FT)=0.006; risk ratio=2.7, 95% confidence interval 1.36; 5.36). The most of children with BPD and the most of healthy preterm infants had the usual genotypes MnSOD 58 Ile/Ile (90% and 98.9% respectively, FT=1.000) and MnSOD 60 Leu/Leu (90% and 96.5% respectively, FT=1.000).
Conclusions: The carriage of MnSOD 16 Ala/Val mutation could be considered as risk factor of the BPD development.
Footnotes
Cite this article as: European Respiratory Journal 2018 52: Suppl. 62, OA307.
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- Copyright ©the authors 2018