title: Chronic exposure to microcystin-LR affected mitochondrial DNA maintenance and caused pathological changes of lung tissue in mice.
abstract: Microcystin-LR (MC-LR), an important variant of cyanotoxin family, was frequently encountered in the contaminated aquatic environment and taken as a potent hepatotoxin. However, a little was known on the association between the long-term MC-LR exposure and lung damage. In this study, we investigated the changes of the pulmonary histopathology, mitochondrial DNA (mtDNA) integrity and the expression of mtDNA encoded genes in the mice with chronic exposed to MC-LR at different concentrations (1, 5, 10, 20 and 40 μg/L) for 12 months. Our results showed that the long-term and persistent exposure to MC-LR disturbed the balance of redox system, influenced mtDNA stability, changed the expression of mitochondrial genes in the lung cells. Notably, MC-LR exposure influenced the level of inflammatory cytokines and resulted in thickening of the alveolar septa. In conclusion, chronic exposure to MC-LR affected mtDNA maintenance, and caused lung impairment in mice.
authors.affiliation: Department of Medical Genetics, Nanjing University School of Medicine, Nanjing, 210093, China; Jiangsu Key Laboratory of Molecular Medicine, Nanjing University School of Medicine, Nanjing, 210093, China.
authors.forename: Xinxiu
authors.initials: X
authors.lastname: Li
authors.affiliation: Department of Medical Genetics, Nanjing University School of Medicine, Nanjing, 210093, China; Jiangsu Key Laboratory of Molecular Medicine, Nanjing University School of Medicine, Nanjing, 210093, China.
authors.forename: Lizhi
authors.initials: L
authors.lastname: Xu
authors.affiliation: Department of Medical Genetics, Nanjing University School of Medicine, Nanjing, 210093, China; Jiangsu Key Laboratory of Molecular Medicine, Nanjing University School of Medicine, Nanjing, 210093, China.
authors.forename: Wei
authors.initials: W
authors.lastname: Zhou
authors.affiliation: Department of Medical Genetics, Nanjing University School of Medicine, Nanjing, 210093, China; Jiangsu Key Laboratory of Molecular Medicine, Nanjing University School of Medicine, Nanjing, 210093, China.
authors.forename: Qingya
authors.initials: Q
authors.lastname: Zhao
authors.affiliation: Department of Medical Genetics, Nanjing University School of Medicine, Nanjing, 210093, China; Jiangsu Key Laboratory of Molecular Medicine, Nanjing University School of Medicine, Nanjing, 210093, China. Electronic address: wangyap@nju.edu.cn.
authors.forename: Yaping
authors.initials: Y
authors.lastname: Wang
mesh_terms: D000818:Animals; D004272:DNA, Mitochondrial / Q000235:genetics / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D008168:Lung / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D008297:Male; D008387:Marine Toxins; D051379:Mice; D008810:Mice, Inbred C57BL; D052998:Microcystins / Q000633:toxicity*; D010084:Oxidation-Reduction / Q000187:drug effects; D014873:Water Pollutants / Q000633:toxicity
chemical_list: D004272:DNA, Mitochondrial; D008387:Marine Toxins; D052998:Microcystins; D014873:Water Pollutants; C057862:cyanoginosin LR
keywords: Lung; Microcystin-LR; Mitochondria; mtDNA