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

Chen, Chuanyue; Liu, Wanjing; Wang, L.; Li, Jian; Chen, Yuanyuan; Jin, Jienan; Kawan, Atufa; Zhang, Xuezhen

doi:10.1016/j.toxicon.2016.04.030

Cited by 68 publications

(29 citation statements)

References 53 publications

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“…Industrialization and urbanization have led to a substantial amount of industrial and domestic wastewater being discharged into natural water resources worldwide, resulting in increasingly serious levels of eutrophication . Cyanobacteria (also known as Cyanophyceae ) are photosynthetic organisms that can proliferate in marine and freshwater environments with high loads of nutrients (e. g., nitrogen and phosphorus compounds), attributable to anthropogenic enrichment . The rapid proliferation of cyanobacteria in marine and freshwater environments is of particular concern for human and ecosystem health because of the potential for bloom‐forming taxa to produce toxins.…”

Section: Introductionmentioning

confidence: 99%

“…Cyanobacterial blooms can further decrease water quality and increase health risks through the production of odorous substances, the induction of oxygen depletion during decomposition and the production of toxins, posing a health hazard not only to aquatic animals but also to humans. The proliferation of cyanobacteria leads to the presence of a variety of harmful substances, including microcystins (MCs), and the human health risk from cyanotoxinsis commonly associated with their ingestion or inhalation during recreational activities .…”

Section: Introductionmentioning

confidence: 99%

“…MCs are a large group of cyclic heptapeptides, with more than 100 structural variants. MC‐LR contains Leucine amino acid and an arginine amino acid in variable positions, and it is the most common and toxic variant .…”

Section: Introductionmentioning

confidence: 99%

“…The toxicity of MCs is due to their strong binding and inhibition of protein phosphatases. They promote the growth of tumors, having a genotoxic effect as well as strong mutagenicity, and cause serious damage to the liver . Due to their high toxicity and potential risk to human health, even at low concentrations, it is of great importance to develop a sensitive, specific, simple and rapid method for the monitoring of MC‐LR in water bodies.…”

Section: Introductionmentioning

confidence: 99%

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Direct Electrochemical Nano‐immunosensor for Microcystin‐LR in Seawater

et al. 2018

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Microcystins are potent hepatotoxins produced by cyanobacteria, which proliferate in wastewaters with high nutrient content. Due to their high toxicity and potential risk to human health, even at low concentrations, the development of a sensitive and rapid method for the monitoring of microcystin‐LR (MC‐LR) in water samples is of great importance. In this context, a new direct electrochemical nano‐immunosensor for MC‐LR detection using the liquid crystal (E)‐1‐decyl‐4‐[(4‐decyloxyphenyl)diazenyl]pyridinium bromide (Br‐Py) as a redox probe and gold nanoparticles stabilized in bovine serum albumin (AuNP‐BSA) is described herein. The microcystin‐LR antibody (anti‐MC‐LR) was covalently immobilized using N‐(3‐dimethylaminopropyl)‐N‐ethylcarbodiimide hydrochloride (EDC) and N‐hydroxysuccinimide (NHS) on an AuNP‐BSA/BrPy film. The proposed sensor response is based on the inhibition of the Br‐Py electrochemical signal after the specific interaction of MC‐LR with immobilized anti‐MC‐LR on the electrode surface. The electrochemical behavior of the immunosensor was studied by square‐wave voltammetry (SWV) and electrochemical impedance spectroscopy (EIS). Under optimized conditions, using SWV and an incubation time of 15 min, the immunosensor exhibits a linear response to MC‐LR concentrations of 0.05 to 500.0 ng mL−1 with a detection limit of 0.05 ng mL−1. The anti‐MC‐LR/AuNP‐BSA/Br‐Py/GCE was successfully applied in the determination of MC‐LR in spiked seawater samples.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Direct Electrochemical Nano‐immunosensor for Microcystin‐LR in Seawater

et al. 2018

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“…Among those isomers, microcystin‐LR (MC‐LR) was considered the most virulent and has been the most studied MC . MC‐LR induces multiple organ toxicities, such as in the liver, heart, intestine, kidney, and reproductive organs …”

Section: Introductionmentioning

confidence: 99%

p53‐Dependent pathway and the opening of mPTP mediate the apoptosis of co‐cultured Sertoli‐germ cells induced by microcystin‐LR

Liu

Huang

et al. 2019

Environmental Toxicology

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Microcystin‐LR (MC‐LR), a potent endotoxin, can induce reproductive toxicity. In order to investigate the role and mechanisms of apoptosis (p53‐dependent and mitochondrial pathways) of germ cells induced by MC‐LR, the co‐cultured primary Sertoli‐germ cells from Sprague‐Dawley rats were used for the experiments. Expression levels of proteins, genes, and mitochondrial membrane potential (MMP) were obtained after exposing co‐cultured Sertoli‐germ cells to MC‐LR with or without the addition of the p53 inhibitor, pifithrin‐α (PFT‐α), and MMP inhibitor, cyclosporin A (CsA). Results indicated that MC‐LR could activate p53‐dependent pathway‐associated proteins in Sertoli‐germ cells, leading to a decrease in MMP (indicating the opening of mitochondrial permeability transition pore [mPTP] and the release of Cytochrome‐c [Cyt‐c]) from the mitochondria into the cytoplasm and eventually the induction of apoptosis. PFT‐α inhibited the expression ofp53, ameliorated the MMP of the co‐cultured Sertoli‐germ cells, and prevented the release of Cyt‐c from the mitochondria into the cytoplasm, which reduces the occurrence of apoptosis. Similarly, the decreased release of Cyt‐c from the mitochondria into the cytoplasm and the declined level of apoptosis in Sertoli‐germ cells induced by MC‐LR were observed after the addition of CsA. These results indicated that the apoptosis of the co‐cultured Sertoli‐germ cells induced by MC‐LR was mediated by the p53‐dependent pathway, with the involvement of the opening of mPTP.

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