Table 3.

Summary of studies on the relationship between acute lung injury and DNA damage/DNA repair mechanisms.

First author	Title	Reference	Observations and Conclusion
Fu H 2017	Calcitonin gene-related peptide protects type II alveolar epithelial cells from hyperoxia-induced DNA damage and cell death	Exp Ther Med 13 (4) 1279-1284	Exposure to 60% oxygen for 24 h predisposes to oxidative damage in cells of the alveolar epithelium, including DNA damage and apoptosis; however, the peptide related to the exogenous calcitonin gene attenuated the hyperoxic lesion and exerted a cytoprotective effect, suggesting that the positive regulation of expression may represent an alternative for the prevention of hyperoxia-induced lung injury.
Barker GF 2006	DNA damage induced by hyperoxia: quantitation and correlation with lung injury	Am J Respir Cell Mol Biol 35 (3) 77-288	Exposure to oxygen caused damage to the DNA base of lung cells as a primary effect of the attack of reactive oxygen species on DNA, which implies the ability of inhaled oxidants to alter the lung genome. Prolonged exposure led to DNA tape breaks suggesting that a side effect of activated nucleases during cell death is likely and correlated with lung disease progression, suggesting that cell injury plays a key role in oxygen pulmonary toxicity.
Wan R 2017	Cobalt nanoparticles induce lung injury, DNA damage and mutations in mice	Part Fibre Toxicol 14 (1) 38	Exposure to cobalt nanoparticles caused oxidative stress, inflammation and lung injury and cell proliferation, which resulted in DNA damage and DNA mutation with great frequency, especially in the G:C to T:A transversion, which can be explained by the greater formation of 8-OHdG induced by the nanoparticles.
Simmons JD 2017	Potential contribution of mitochondrial DNA damage associated molecular patterns in transfusion products to the development of acute respiratory distress syndrome after multiple transfusions	J Trauma Acute Care Surg 82 (6) 1023-1029	Fresh frozen plasma and platelets contain large amounts of extracellular mitochondrial DNA (mtDNA) that the amount of mAMDs associated with mtDNA administered during transfusion may be a contributor to serum mtDNA DAMP levels, and that serum levels of mtDNA DAMPs after multiple transfusions may predict the development of ARDS. Therefore, serum measurements of mtDNA DAMP may be predictive biomarkers for the evolution of ARDS.
Lee YL 2017	Mitochondrial DNA Damage Initiates Acute Lung Injury and Multi-Organ System Failure Evoked in Rats by Intra-Tracheal Pseudomonas Aeruginosa	Shock 48 (1) 54-60	mt-targeted Ogg1 suppresses bacterial-induced lung tissue mtDNA damage and ALI accompanied by attenuation of multiple organ failure and lethality is strong evidence that mitochondrial genomic integrity is a critical step driving injury propagation.
Sergio LPS 2019	Low-power laser alters mRNA levels from DNA repair genes in acute lung injury induced by sepsis in Wistar rats.	Lasers Med Sci. 34 (1) 157-168	Acute lung injury alters the mRNA levels of DNA repair genes, understanding that it would be part of the cellular response to sepsis, and after treatment with low-power infrared laser, mRNA levels of DNA repair genes are modulated in lung injury acute.