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Pathological damage and immunomodulatory effects of zebrafish exposed to microcystin-LR

Cyanobacterial blooms caused by water eutrophication have become a worldwide problem. Microcystins (MCs), especially microcystin-LR (MC-LR), released during cyanobacterial blooms exert great toxicity on fish and even lead to massive death. The present study mainly investigated the pathological damag...

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Published in:Toxicon (Oxford) 2016-08, Vol.118, p.13-20
Main Authors: Chen, Chuanyue, Liu, Wanjing, Wang, Li, Li, Jian, Chen, Yuanyuan, Jin, Jienan, Kawan, Atufa, Zhang, Xuezhen
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description Cyanobacterial blooms caused by water eutrophication have become a worldwide problem. Microcystins (MCs), especially microcystin-LR (MC-LR), released during cyanobacterial blooms exert great toxicity on fish and even lead to massive death. The present study mainly investigated the pathological damage and immune response of spleen, gut and gill in zebrafish exposed to MC-LR. Fish were exposed to 0, 1, 5 and 20 μg/L of MC-LR for 30 d. In zebrafish exposed to 5 and 20 μg/L MC-LR, edematous mitochondria, deformation of the nucleus and compaction of chromatin were observed in lymphocyte of spleen; frayed gut villi, exfoliation of epithelial cells and widespread cell lyses were observed in intestines; hyperemia in gill lamellae, epithelial tissue edema and uplift and lamellar fusion were observed in gill. Varied changed gene expression was observed in spleen, intestine and gill of zebrafish. The transcriptional levels of IFN-1 and IL-8 in spleen significantly up-regulated in 20 μg/L group, and the transcription of IL-1β and TNFα in spleen increased in 1 μg/L MC-LR treated fish. In addition, the mRNA levels of IFN-1, IL-1β, IL-8, TGF-β and TNF-α dramatically increased in intestine and gill in all MC-LR treated groups. The present studies indicated that MC-LR exposure caused marked pathological damage, however, fish could adjust actively the expression of innate immune-related genes to resist the tissue damage. Our findings provided strong evidence of the recovery potential of fish exposed to microcystins. •Subchronic exposure of microcystin-LR causes marked pathological damage in spleen, intestine and gill.•Fish increase the transcriptional levels of innate immune-related genes to resist the tissue damage.•Fish exhibit a recovery potential after MC-LR exposure.•There is a contradiction between the damaged tissues and activated immune genes in fish caused by MC-LR exposure.
doi_str_mv 10.1016/j.toxicon.2016.04.030
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Microcystins (MCs), especially microcystin-LR (MC-LR), released during cyanobacterial blooms exert great toxicity on fish and even lead to massive death. The present study mainly investigated the pathological damage and immune response of spleen, gut and gill in zebrafish exposed to MC-LR. Fish were exposed to 0, 1, 5 and 20 μg/L of MC-LR for 30 d. In zebrafish exposed to 5 and 20 μg/L MC-LR, edematous mitochondria, deformation of the nucleus and compaction of chromatin were observed in lymphocyte of spleen; frayed gut villi, exfoliation of epithelial cells and widespread cell lyses were observed in intestines; hyperemia in gill lamellae, epithelial tissue edema and uplift and lamellar fusion were observed in gill. Varied changed gene expression was observed in spleen, intestine and gill of zebrafish. The transcriptional levels of IFN-1 and IL-8 in spleen significantly up-regulated in 20 μg/L group, and the transcription of IL-1β and TNFα in spleen increased in 1 μg/L MC-LR treated fish. In addition, the mRNA levels of IFN-1, IL-1β, IL-8, TGF-β and TNF-α dramatically increased in intestine and gill in all MC-LR treated groups. The present studies indicated that MC-LR exposure caused marked pathological damage, however, fish could adjust actively the expression of innate immune-related genes to resist the tissue damage. 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The transcriptional levels of IFN-1 and IL-8 in spleen significantly up-regulated in 20 μg/L group, and the transcription of IL-1β and TNFα in spleen increased in 1 μg/L MC-LR treated fish. In addition, the mRNA levels of IFN-1, IL-1β, IL-8, TGF-β and TNF-α dramatically increased in intestine and gill in all MC-LR treated groups. The present studies indicated that MC-LR exposure caused marked pathological damage, however, fish could adjust actively the expression of innate immune-related genes to resist the tissue damage. Our findings provided strong evidence of the recovery potential of fish exposed to microcystins. •Subchronic exposure of microcystin-LR causes marked pathological damage in spleen, intestine and gill.•Fish increase the transcriptional levels of innate immune-related genes to resist the tissue damage.•Fish exhibit a recovery potential after MC-LR exposure.•There is a contradiction between the damaged tissues and activated immune genes in fish caused by MC-LR exposure.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>27085306</pmid><doi>10.1016/j.toxicon.2016.04.030</doi><tpages>8</tpages></addata></record>
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source ScienceDirect Journals
subjects Animals
Bacterial Toxins - toxicity
Blooms
Damage
Danio rerio
Drug Resistance
Exposure
Fish
Gene expression
Gene Expression Regulation - drug effects
Gills - drug effects
Gills - immunology
Gills - metabolism
Gills - ultrastructure
Immunity
Immunity, Innate - drug effects
Immunity, Mucosal - drug effects
Inflammation Mediators - agonists
Inflammation Mediators - metabolism
Intestinal Mucosa - drug effects
Intestinal Mucosa - immunology
Intestinal Mucosa - metabolism
Intestinal Mucosa - ultrastructure
Intestines
Microcystin-LR
Microcystins - toxicity
Microscopy, Electron, Scanning
Microvilli - drug effects
Microvilli - immunology
Microvilli - metabolism
Microvilli - ultrastructure
Organ Specificity
Osmolar Concentration
Pathological damage
Random Allocation
Recovery
RNA, Messenger - metabolism
Spleen
Spleen - drug effects
Spleen - immunology
Spleen - metabolism
Spleen - ultrastructure
Water Pollutants, Chemical - toxicity
Zebrafish
Zebrafish Proteins - agonists
Zebrafish Proteins - genetics
Zebrafish Proteins - metabolism
title Pathological damage and immunomodulatory effects of zebrafish exposed to microcystin-LR
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