Factors Of Postnatal Hyperoxia And Premature Aging

Postnatal Hyperoxia and Premature Aging It is known that hyperoxic exposure through oxygen supplementation results in increased levels of reactive oxygen species which can subsequently damage DNA (O’Reilly, 2001). Telomere sequences protect the end of DNA and these will decrease upon DNA replication thereby limiting the capacity of cells to proliferate. Attrition of telomeres is a characteristic of aging and serves as a major marker of premature aging regardless of phenotype (Lopez-Otin, 2013). There are several studies that suggest that shorter telomere lengths can be found in circulating leukocytes of young adults born preterm as compared to term born controls and while this has not be implicated as a general association between telomere†¦show more content†¦There are numerous lung disease states in which aberrant protein homeostasis is implicated, both in pediatrics and adults. Within the lung, there is data suggesting that protein degradation pathways are dysregulated by hyperoxia and mechanical ventila tion through reactive oxygen species production which can be especially challenging to an immature lung (Berkelhamer, 2013; Birukov, 2009). It is not known whether protein degradation alterations have been implicated within the right heart as well. It is unknown to whether mechanical ventilation and hyperoxia trigger autophagy or proteasome dysfunction in infants. In adult mice however, autophagy within the lungs is increased with mechanical ventilation (Lopez-Alonso, 2013). Hyperoxia has also been shown to alter autophagy through induction of autophagosome formation within bronchial epithelial cells (Tanaka, 2012). The implication that protein degradation pathways are dysregulated by hyperoxia is especially important given that not only is it implicated in aging within the lung, but that the mitochondrial dysregulation not only seen at work within this body of literature, but also the right ventricles used in this study would suggest that protein degradation could play a role in the right ventricular dysfunction found after exposure to post-natal hyperoxia (Goss, 2017).