N-acetylcysteine modulates redox imbalance and inflammation in macrophages and mice exposed to formaldehyde.

IF 3.6 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY
Free Radical Research Pub Date : 2023-05-01 Epub Date: 2023-12-26 DOI:10.1080/10715762.2023.2284636
Elena Cecilia Marcano-Gómez, Ana Beatriz Farias de Souza, Pedro Alves Machado-Junior, Andrea Jazel Rodríguez-Herrera, Thalles de Freitas Castro, Sirlaine Pio Gomes da Silva, Ramony Gonzaga Vieira, André Talvani, Katiane de Oliveira Pinto Coelho Nogueira, Laser Antônio Machado de Oliveira, Frank Silva Bezerra
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引用次数: 0

Abstract

This 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.

n -乙酰半胱氨酸调节甲醛暴露的巨噬细胞和小鼠的氧化还原失衡和炎症。
本研究旨在评价n -乙酰半胱氨酸(NAC)对甲醛暴露的细胞和小鼠的保护作用。体外实验用J774A。将1个巨噬细胞与甲醛或NAC孵育8、16和24 h,评估细胞活力和活性氧(ROS)。在体内实验中,将48只C57BL/6小鼠分为对照组(CG)、对照组(VG)、对照组(VG)、甲醛暴露组(FG)和甲醛暴露组(FN100、FN150、FN200) NAC剂量分别为100、150、200 mg/Kg,为期5 d。在体外,甲醛促进了细胞活力的降低和ROS的增加,而NAC则减少了甲醛诱导的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较高,并促进炎症标志物IL-6、IL-15和IL-10的分泌。甲醛暴露还促进了氧化还原失衡和氧化损伤,表现为超氧化物歧化酶、过氧化氢酶活性升高,GSH/GSSG比值降低,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。综上所述,在体外和体内模型中,NAC均具有保护作用,可调节炎症反应和氧化还原失衡,从而预防甲醛暴露引起的气道损伤。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Free Radical Research
Free Radical Research 生物-生化与分子生物学
CiteScore
6.70
自引率
0.00%
发文量
47
审稿时长
3 months
期刊介绍: Free Radical Research publishes high-quality research papers, hypotheses and reviews in free radicals and other reactive species in biological, clinical, environmental and other systems; redox signalling; antioxidants, including diet-derived antioxidants and other relevant aspects of human nutrition; and oxidative damage, mechanisms and measurement.
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