The toxic effects of microcystin-LR on mouse lungs and alveolar type II epithelial cells

Cong Wang, Shen Gu, Xiaoqin Yin, Mingming Yuan, Zou Xiang, Zutong Li, Honghui Cao, Xiannan Meng, Kebin Hu, Xiaodong Han

Research output: Contribution to journalArticle

8 Citations (Scopus)

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 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. 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.

Original languageEnglish (US)
Pages (from-to)81-88
Number of pages8
JournalToxicon
Volume115
DOIs
StatePublished - Jun 1 2016

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Alveolar Epithelial Cells
Poisons
Leucine
Arginine
Lung
Intercellular Junctions
microcystin
cyanoginosin LR
Epithelial Cells
Tissue
Apoptosis
Pulmonary Atelectasis
Blood Circulation
Hemodynamics
Cyanobacteria
Lung Injury
Cell Survival
Cells

All Science Journal Classification (ASJC) codes

  • Toxicology

Cite this

Wang, Cong ; Gu, Shen ; Yin, Xiaoqin ; Yuan, Mingming ; Xiang, Zou ; Li, Zutong ; Cao, Honghui ; Meng, Xiannan ; Hu, Kebin ; Han, Xiaodong. / The toxic effects of microcystin-LR on mouse lungs and alveolar type II epithelial cells. In: Toxicon. 2016 ; Vol. 115. pp. 81-88.
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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 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. 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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Wang, C, Gu, S, Yin, X, Yuan, M, Xiang, Z, Li, Z, Cao, H, Meng, X, Hu, K & Han, X 2016, 'The toxic effects of microcystin-LR on mouse lungs and alveolar type II epithelial cells', Toxicon, vol. 115, pp. 81-88. https://doi.org/10.1016/j.toxicon.2016.03.007

The toxic effects of microcystin-LR on mouse lungs and alveolar type II epithelial cells. / Wang, Cong; Gu, Shen; Yin, Xiaoqin; Yuan, Mingming; Xiang, Zou; Li, Zutong; Cao, Honghui; Meng, Xiannan; Hu, Kebin; Han, Xiaodong.

In: Toxicon, Vol. 115, 01.06.2016, p. 81-88.

Research output: Contribution to journalArticle

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AU - Wang, Cong

AU - Gu, Shen

AU - Yin, Xiaoqin

AU - Yuan, Mingming

AU - Xiang, Zou

AU - Li, Zutong

AU - Cao, Honghui

AU - Meng, Xiannan

AU - Hu, Kebin

AU - Han, Xiaodong

PY - 2016/6/1

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N2 - 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 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. 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.

AB - 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 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. 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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