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1.	Wang, C., et al. (author) The toxic effects of microcystin-LR on mouse lungs and alveolar type II epithelial cells 2016 In: Toxicon. - : Elsevier BV. - 0041-0101. ; 115, s. 81-88 Journal article (peer-reviewed)abstract Objectives: 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). Methods: MC-LR was orally administered to mice at 0, 1, 10, and 40 mu g/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. Results: 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. Conclusions: These data support the toxic potential of low-dose MC-LR in rendering chronic injury to lung tissues.

Wang, C., et al. (author)
The toxic effects of microcystin-LR on mouse lungs and alveolar type II epithelial cells
2016
In: Toxicon. - : Elsevier BV. - 0041-0101. ; 115, s. 81-88
Journal article (peer-reviewed)abstract
- Objectives: 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). Methods: MC-LR was orally administered to mice at 0, 1, 10, and 40 mu g/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. Results: 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. Conclusions: These data support the toxic potential of low-dose MC-LR in rendering chronic injury to lung tissues.

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