Camila Freitas dos Santos ,Mariana Gobbo Braz ,Nayara Micarelli de Arruda ,Laura Caram ,Duelene Ludimila Nogueira ,Suzana Erico Tanni,Irma de Godoy ,Renata Ferrari
Chronic obstructive pulmonary disease (COPD) is characterized by chronic inflammation of the lower airways, and COPD patients show two to five times higher risk of lung cancer than smokers with normal lung function. COPD is associated with increased oxidative stress, which may cause DNA damage and lung carcinogenesis. Our aim was to evaluate DNA damage and oxidative stress (lipid peroxidation and antioxidant status) and their relationship in patients with COPD with and without lung cancer.
The driving forces behind cancer are gene, nucleotide, and cellular structure changes. Somatic cells can acquire mutations one or two orders of magnitude more quickly than germline cells, making them more susceptible to different types of cancer. The vast majority of these mutations, called passenger, have little effect on cell proliferation compared to a few driver mutations that give cells a selective advantage.
Materials and Methods:
We evaluated 18 patients with COPD, 18 with COPD with lung cancer, and 18 controls (former or current smokers). DNA damage was evaluated in peripheral blood lymphocytes using a comet assay; the concentration of malondialdehyde (MDA) and hydrophilic antioxidant performance (HAP) were measured in the plasma.
Our findings showed that patients with COPD and lung cancer presented increased levels of DNA damage determined by the comet assay when compared to the controls. The percentage of HAP was lower in patients who had an association of lung cancer and COPD, than in those in the other two groups. DNA strand breaks and MDA levels showed a positive association with interaction COPD and cancer in the multiple linear regression analysis; in contrast, HAP showed a negative association.
Citation: dos Santos CF, Braz MG, de Arruda NM, Caram L, Nogueira DL, Tanni SE, et al. (2022) DNA damage and antioxidant capacity in COPD patients with and without lung cancer. PLoS ONE 17(11): e0275873. https://doi.org/10.1371/journal.pone.0275873
Editor: Emre Avci, University of Health Sciences Gulhane Faculty of Pharmacy, TURKEY
Received: January 8, 2022; Accepted: September 23, 2022; Published: November 3, 2022.
Copyright: © 2022 dos Santos et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Data Availability: The data cannot be shared due to potentially identifying or sensitive information. Future researchers will be able to request the data used in this study through the contact of the local ethics committee of São Paulo State University: Chácara Butignolli, s / n, Botucatu, São Paulo - Brazil. Zip code: 18618970. telephone: 3880-1609. email: email@example.com. Additionally, the study ethics approval may be requested through the conep portal (https://Plataformabrasil.saude.gov.br/).
Funding: Renata Ferrari: This work was supported by the National Council for Scientific and Technological Development (Conselho Nacional de Desenvolvimento Científico e Tecnológico - CNPq) [grant numbers 470496/2014-2]. Camila Freitas dos Santos: This work was supported by São Paulo Research Foundation (Fundação de Amparo à Pesquisa do Estado de São Paulo - FAPESP) [grant numbers 2019/15075-2].
Competing interests: The authors have declared that no competing interests exist.