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The toxic effects of microcystin-LR on mouse lungs and alveolar type II epithelial cells
Microcystin-leucine arginine (MC-LR) is produced by cyanobacteria and can accumulate in lungs through blood circulation. However, the effect of MC-LR on lung remains unclear. In this study, we investigated the chronic, low-dose effect of MC-LR on mouse lung tissues and the influence of MC-LR on mous...
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Published in: | Toxicon (Oxford) 2016-06, Vol.115, p.81-88 |
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Main Authors: | , , , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Microcystin-leucine arginine (MC-LR) is produced by cyanobacteria and can accumulate in lungs through blood circulation. However, the effect of MC-LR on lung remains unclear. In this study, we investigated the chronic, low-dose effect of MC-LR on mouse lung tissues and the influence of MC-LR on mouse alveolar type II epithelial cells (ATII cells).
MC-LR was orally administered to mice at 0, 1, 10, and 40 μg/L for 6 consecutive months and mouse lungs were obtained for histopathological and immunoblot analysis. ATII cells were cultured in various concentrations of MC-LR (0, 0.5, 5, 50, 500 nmol/L) for indicated time and the cell viability and proteins change were tested.
Our study revealed that the chronic, low-dose MC-LR exposure induced alveolar collapse and lung cell apoptosis as well as the breach of cell junction integrity. Furthermore, following treatment with MC-LR, ATII cells could uptake MC-LR, resulting in apoptosis and disruption of cell junction integrity.
These data support the toxic potential of low-dose MC-LR in rendering chronic injury to lung tissues.
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•Chronic low-dose exposure to MC-LR was toxic to lung.•MC-LR could induce the decrease of cell-to-cell communication in mouse lung.•MC-LR suppress the activity of ATII cells.•Intercellular junctions were decreased with the increase concentration of MC-LR. |
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ISSN: | 0041-0101 1879-3150 |
DOI: | 10.1016/j.toxicon.2016.03.007 |