氧化应激
超氧化物歧化酶
化学
脂质过氧化
活性氧
过氧化氢酶
甲醛
炎症
支气管肺泡灌洗
乙酰半胱氨酸
药理学
体内
活力测定
谷胱甘肽
体外
生物化学
免疫学
抗氧化剂
医学
生物
内科学
肺
酶
生物技术
作者
Elena Cecilia Marcano-Gómez,Ana Beatriz Farias de Souza,Pedro Alves Machado-Júnior,Andrea Jazel Rodríguez-Herrera,Thalles de Freitas Castro,Sirlaine Pio Gomes da Silva,Reinaldo Wilson Vieira,André Talvani,Katiane de Oliveira Pinto Coelho Nogueira,Laser Antônio Machado Oliveira,Frank Silva Bezerra
标识
DOI:10.1080/10715762.2023.2284636
摘要
AbstractThis study aimed to evaluate the protective role of N-acetylcysteine (NAC) in cells and mice exposed to formaldehyde. For the in vitro study, J774A.1 macrophages cells were incubated for 8, 16 and 24 h with formaldehyde or NAC to assess cell viability and reactive oxygen species (ROS). In the in vivo study, C57BL/6 mice (n = 48) were divided into 6 groups: control (CG), vehicle (VG) that received saline by orogastric gavage, a group exposed to formaldehyde 1% (FG) and formaldehyde exposed groups that received NAC at doses of 100, 150 and 200 mg/Kg (FN100, FN150 and FN200) for a period of 5 days. In vitro, formaldehyde promoted a decrease in cell viability and increased ROS, while NAC reduced formaldehyde-induced ROS production. Animals exposed to formaldehyde presented higher leukocyte counts in the blood and in the bronchoalveolar lavage fluid, and promoted secretion of inflammatory markers IL-6, IL-15, and IL-10. The exposure to formaldehyde also promoted redox imbalance and oxidative damage characterized by increased activities of superoxide dismutase, catalase, decreased GSH/GSSG ratio, as well as it increased levels of protein carbonyls and lipid peroxidation. NAC administration after formaldehyde exposure attenuated oxidative stress markers, secretion of inflammatory mediators and lung inflammation. In conclusion, both in in vitro and in vivo models, NAC administration exerted protective effects, which modulated the inflammatory response and redox imbalance, thus preventing the development airway injury induced by formaldehyde exposure.Keywords: N-acetylcysteineformaldehydeoxidative stressinflammationlung AcknowledgmentsThe authors thank Michel Oliveira and Yannick Diedrich for their technical assistance during this study.Disclosure statementNo potential conflict of interest was reported by the author(s).Additional informationFundingThe authors are thankful to Financiadora de Estudos e Projetos (Study and Project Financing Institution) – FINEP; Fundação de Amparo à Pesquisa de Minas (Foundation for Research Support of Minas Gerais) (FAPEMIG) [FAPEMIG – n° APQ − 02511-22] and Conselho Nacional de Desenvolvimento Científico e Tecnológico (National Council for Scientific and Technological Development (CNPq) [CNPq – n° 305385/2021-6, nº 305634/2017-8].
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