• Luiz Philippe da Silva Sergio, Andre Luiz Mencalha, Adenilson de Souza da Fonseca, and Flavia de Paoli.
• Departamento de Biofísica e Biometria, Instituto de Biologia Roberto Alcantara Gomes, Universidade do Estado do Rio de Janeiro, Boulevard Vinte e Oito de Setembro, 87, Vila Isabel, Rio de Janeiro, 20551030, Brazil. Electronic address: luizphilippesergio@gmail.com.
• Biomed. Pharmacother. 2019 Nov 1; 119: 109412.

AbstractAcute pulmonary injury, or acute respiratory distress syndrome, has a high incidence in elderly individuals and high mortality in its most severe degree, becoming a challenge to public health due to pathophysiological complications and increased economic burden. Acute pulmonary injury can develop from sepsis, septic shock, and pancreatitis causing reduction of alveolar airspace due to hyperinflammatory response. Oxidative stress acts directly on the maintenance of inflammation, resulting in tissue injury, as well as inducing DNA damages. Once the DNA is damaged, enzymatic DNA repair mechanisms act on lesions in order to maintain genomic stability and, consequently, contribute to cell viability and homeostasis. Although palliative treatment based on mechanical ventilation and antibiotic using have a kind of efficacy, therapies based on modulation of DNA repair and genomic stability could be effective for improving repair and recovery of lung tissue in patients with acute pulmonary injury.Copyright © 2019 The Authors. Published by Elsevier Masson SAS.. All rights reserved.

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