Chronic exposure to microcystin-LR affected mitochondrial DNA maintenance and caused pathological changes of lung tissue in mice

• Published in: Environmental pollution (1987) 2016-03, Vol.210, p.48-56
• Main Authors: Li, Xinxiu, Xu, Lizhi, Zhou, Wei, Zhao, Qingya, Wang, Yaping
• Format: Article
• Language: English
• Subjects: Animals; DNA, Mitochondrial - genetics; DNA, Mitochondrial - metabolism; Dose-Response Relationship, Drug; Lung; Lung - drug effects; Lung - metabolism; Lung - pathology; Male; Mice; Mice, Inbred C57BL; Microcystin-LR; Microcystins - toxicity; Mitochondria; mtDNA; Oxidation-Reduction - drug effects; Water Pollutants - toxicity
• ISSN: 0269-7491; 1873-6424
• DOI: 10.1016/j.envpol.2015.12.001

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. •A simulated natural exposure to MC-LR caused the lung pathological changes.•The chronic exposure disturbed the redox system balance of lung tissue cells.•The chronic exposure impaired the mtDNA stability and mitochondria function.•The lung was one of the vulnerable organs to MC-LR exposure in mice. Long-term exposure to MC-LR in drinking water disturbed the balance of redox system, affected mitochondrial DNA maintenance and caused lung impairment in mice.