Microcystins distribution, bioaccumulation, and Microcystis genotype succession in a fish culture pond

Bi, Xiangdong; Dai, Wei; Shao-jie, Dong; Zhang, Shulin; Zhang, Dajuan; Wu, Miao

doi:10.1016/j.scitotenv.2019.06.156

Cited by 47 publications

(10 citation statements)

References 61 publications

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“…Despite these high MC concentrations, almost all MC was covalently bound with approximately 0.007 and 0.03%, respectively, being freely available; it is unknown if covalently bound MC is biologically available when larvae are consumed, and within the context of NPLD, whether covalently bound MC participates in the aetiology of NPLD (Williams et al., 1997). Bioaccumulation and biomagnification of MC by plants (Cao et al., 2019) and animals (Ger et al., 2018; Miller et al., 2010; Zhang et al., 2009) throughout food webs (Pham & Utsumi, 2018) is known to occur and can negatively impact fish health (Bi et al., 2019; Vasconcelos et al., 2013; Zamora‐Barrios et al., 2019). Dietary consumption should be further investigated as an avenue of algal toxin exposure, including MC, and as a potential cause of NPLD.…”

Section: Discussionmentioning

confidence: 99%

Acute microcystin exposure induces reversible histopathological changes in Chinook Salmon (Oncorhynchus tshawytscha) and Atlantic Salmon (Salmo salar)

Shartau

Snyman

Turcotte

et al. 2022

Journal of Fish Diseases

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Atlantic Salmon (Salmo salar) and Chinook Salmon (Oncorhynchus tshawytscha) develop a severe liver disease called net-pen liver disease (NPLD), which is characterized by hepatic lesions that include megalocytosis and loss of gross liver structure. Based on studies where salmonids have been exposed to microcystin (MC) via intraperitoneal injection, NPLD is believed to be caused by MC exposure, a hepatotoxin produced by cyanobacteria. Despite the link between MC and NPLD, it remains uncertain if environmentally relevant MC exposure is responsible for NPLD. To determine if we could produce histopathology consistent with NPLD, we compared the response of Atlantic and Chinook Salmon sub-lethal MC exposure. Salmon were orally gavaged with saline or MC containing algal paste and sampled over 2 weeks post-exposure. Liver lesions appeared by 6 h but were resolved 2-weeks post-exposure; histopathological changes observed in other tissues were not as widespread, nor was their severity as great as those in the liver. There was no evidence for NPLD due to the absence of hepatic megalocytosis. These results indicate that the development of NPLD is not due to acute MC exposure but may be associated with higher MC concentration occurring in food, long-term exposure through drinking of contaminated seawater and/or interactions with other marine toxins.

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Section: Discussionmentioning

confidence: 99%

Acute microcystin exposure induces reversible histopathological changes in Chinook Salmon (Oncorhynchus tshawytscha) and Atlantic Salmon (Salmo salar)

Shartau

Snyman

Turcotte

et al. 2022

Journal of Fish Diseases

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“…At the same time, content of MC-RR was negatively correlated with content of MC-RR in blood, indicating that blood might play an important role in the transport of MC-RR to renal excretion. In a recent study, Bi et al [48] found that the accumulation of MCs in the liver was the highest, followed by the kidney in the market crucian carp. Jia et al [49] noted that the MCs content in fish varied in different areas of Lake Taihu, China, and the toxins were mainly concentrated in the digestive organs such as liver and kidney when the bioaccumulation of MCs in four species of fish was assessed.…”

Section: Distribution Of Mcs In the Kidneymentioning

confidence: 96%

“…In most cases, MCs are not easily diffused through the plasma membrane owing to their water solubility, high molecular weight and complicated structure. However, several studies have shown that MCs could be detected in the kidney of mammals and fish under natural and laboratory conditions [42][43][44][45][46][47][48][49][50][51]. It is well known that due to the specificity of cells, a specific pathway from MCs to renal cells may exist [52].…”

Section: Distribution Of Mcs In the Kidneymentioning

confidence: 99%

“…Therefore, the systemic distribution of MCs in organs will depend on blood perfusion and the type and expression level of OATP carriers [52,87]. The presence of MCs in the kidney of rodents [42,46] and fishes [48,114] suggests that MCs were able to get across the renal plasma membrane. A meaningful experiment conducted by Sun et al [83] revealed that after exposure to MC-RR, rats and mice showed different outcomes.…”

Section: Cellular Uptake Of Mcsmentioning

confidence: 99%

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A Review of Nephrotoxicity of Microcystins

Liu

et al. 2020

Toxins

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Cyanobacterial blooms triggered by eutrophication and climate change have become a global public health issue. The toxic metabolites microcystins (MCs) generated by cyanobacteria can accumulate in food chain and contaminate water, thus posing a potential threat to human and animals health. Studies have suggested that aside liver, the kidney may be another target organ of MCs intoxication. Therefore, this review provides various evidences on the nephrotoxicity of MCs. The review concludes that nephrotoxicity of MCs may be related to inhibition of protein phosphatases and excessive production of reactive oxygen species, cytoskeleton disruption, endoplasmic reticulum stress, DNA damage and cell apoptosis. To protect human from MCs toxic consequences, this paper also puts forward some directions for further research.

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“…MCs have been intensively studied among cyanotoxins due to their toxicity, causing severe liver and kidney damage, tumor promotion and gastroenteritis [5,6]. Accumulation of MCs in aquatic ecosystems increases public health concerns [7,8].…”

Section: Introductionmentioning

confidence: 99%

A Novel Freshwater Cyanophage, Mae-Yong924-1, Reveals a New Family

Qian

Lin

et al. 2022

Viruses

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Cyanobacterial blooms are a worldwide ecological issue. Cyanophages are aquatic viruses specifically infecting cyanobacteria. Little is known about freshwater cyanophages. In this study, a freshwater cyanophage, Mae-Yong924-1, was isolated by the double-layer agar plate method using Microcystis aeruginosa FACHB-924 as an indicator host. Mae-Yong924-1 has several unusual characteristics: a unique shape, cross-taxonomic order infectivity and a very unique genome sequence. Mae-Yong924-1 contains a nearly spherical head of about 100 nm in diameter. The tail or tail-like structure (approximately 40 nm in length) is like the tassel of a round Chinese lantern. It could lyse six diverse cyanobacteria strains across three orders including Chroococcales, Nostocales and Oscillatoriales. The genome of the cyanophage is 40,325 bp in length, with a G + C content of 48.32%, and 59 predicted open reading frames (ORFs), only 12 (20%) of which were functionally annotated. Both BLASTn and BLASTx scanning resulted in “No significant similarity found”, i.e., the Mae-Yong924-1 genome shared extremely low homology with sequences in NCBI databases. Mae-Yong924-1 formed a root node alone and monopolized a root branch in the proteomic tree based on genome-wide sequence similarities. The results suggest that Mae-Yong924-1 may reveal a new unknown family apparently distinct from other viruses.

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Microcystins distribution, bioaccumulation, and Microcystis genotype succession in a fish culture pond

Cited by 47 publications

References 61 publications

Acute microcystin exposure induces reversible histopathological changes in Chinook Salmon (Oncorhynchus tshawytscha) and Atlantic Salmon (Salmo salar)

Acute microcystin exposure induces reversible histopathological changes in Chinook Salmon (Oncorhynchus tshawytscha) and Atlantic Salmon (Salmo salar)

A Review of Nephrotoxicity of Microcystins

A Novel Freshwater Cyanophage, Mae-Yong924-1, Reveals a New Family

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