Exposure to dibenzofuran triggers autophagy in lung cells

被引:25
作者
Duarte, Filipe V. [1 ]
Teodoro, Joao S. [1 ]
Rolo, Anabela P. [1 ,2 ]
Palmeira, Carlos M. [1 ,3 ]
机构
[1] Univ Coimbra, CNC Ctr Neurosci & Cell Biol, P-3004517 Coimbra, Portugal
[2] Univ Aveiro, Dept Biol, P-3810193 Aveiro, Portugal
[3] Univ Coimbra, Dept Life Sci, Ctr Neurosci & Cell Biol, Fac Sci & Technol, P-3004517 Coimbra, Portugal
关键词
A549; Autophagy; Dibenzofuran; Lung; Mitochondria; REACTIVE OXYGEN PRODUCTION; HYDROCARBON RECEPTOR; LIVER; MITOCHONDRIA; DEATH; CYTOTOXICITY; MECHANISMS; NEURONS; DISEASE; CANCER;
D O I
10.1016/j.toxlet.2011.11.029
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 [卫生毒理学];
摘要
Environmental pollutants, such as dioxins and furans, are extremely toxic and related with pulmonary disease development. Exposure of A549 human lung cells to dibenzofuran showed both time- and concentration-dependent decreases in cell proliferation and MIT reduction, but no alterations in cell viability. No differences were observed in the number of apoptotic nuclei, which can be due to the energetic failure caused by dibenzofuran-induced ATP depletion. Moreover, cells in culture exposed to the pollutant showed an increase in the conversion of LC3, a protein involved in the autophagic process. Incubation of A549 lung cells with dibenzofuran caused an increase in Lysotracker Red staining, indicating an increase in lysosomal vacuoles content. These results suggest that exposure to dibenzofuran affects lung mitochondrial phosphorylative function, causing an increase in the population of dysfunctional mitochondria and an impairment in the energetic status maintenance, therefore stimulating autophagy as a possible rescue mechanism in this cell line. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:35 / 42
页数:8
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