Laboratory of Experimental Pathophysiology, Department of Biological Sciences and Center of Research in Biological Sciences, Federal University of Ouro Preto (UFOP), Ouro Preto, Brazil.
Laboratory of Immunobiology of Inflammation, Department of Biological Sciences, Institute of Exact and Biological Sciences, Federal University of Ouro Preto (UFOP), Ouro Preto, Brazil.
Free Radic Res. 2023 May-Jun;57(6-12):444-459. doi: 10.1080/10715762.2023.2284636. Epub 2023 Dec 26.
This study aimed to evaluate the protective role of N-acetylcysteine (NAC) in cells and mice exposed to formaldehyde. For the 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 study, C57BL/6 mice ( = 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. , 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 and models, NAC administration exerted protective effects, which modulated the inflammatory response and redox imbalance, thus preventing the development airway injury induced by formaldehyde exposure.
本研究旨在评估 N-乙酰半胱氨酸（NAC）对暴露于甲醛的细胞和小鼠的保护作用。为此，将 J774A.1 巨噬细胞分别孵育 8、16 和 24 小时，用甲醛或 NAC 处理，以评估细胞活力和活性氧（ROS）。在本研究中，将 C57BL/6 小鼠（ = 48）分为 6 组：对照组（CG）、给予生理盐水灌胃的载体组（VG）、1%甲醛暴露组（FG）和分别给予 100、150 和 200 mg/kg NAC 的甲醛暴露组（FN100、FN150 和 FN200），为期 5 天。结果显示，甲醛降低了细胞活力并增加了 ROS，而 NAC 减少了甲醛诱导的 ROS 产生。暴露于甲醛的动物血液和支气管肺泡灌洗液中的白细胞计数增加，并促进了炎症标志物 IL-6、IL-15 和 IL-10 的分泌。甲醛暴露还导致氧化还原失衡和氧化损伤，表现为超氧化物歧化酶、过氧化氢酶活性增加，谷胱甘肽/谷胱甘肽过氧化物酶比值降低，以及蛋白质羰基和脂质过氧化水平升高。甲醛暴露后给予 NAC 可减轻氧化应激标志物、炎症介质的分泌和肺部炎症。总之，在体内和体外模型中，NAC 给药均发挥了保护作用，调节了炎症反应和氧化还原失衡，从而防止了甲醛暴露引起的气道损伤的发展。
