microcystin and Fish-Diseases

Cyanobacteria (blue-green algae) have been present on Earth for over 2 billion years, and can produce a variety of bioactive molecules, such as cyanotoxins. Microcystins (MCs), the most frequently detected cyanotoxins, pose a threat to the aquatic environment and to human health. The classic toxic mechanism of MCs is the inhibition of the protein phosphatases 1 and 2A (PP1 and PP2A). Immunity is known as one of the most important physiological functions in the neuroendocrine-immune network to prevent infections and maintain internal homoeostasis in fish. The present review aimed to summarize existing papers, elaborate on the MC-induced immunotoxicity in fish, and put forward some suggestions for future research. The immunomodulatory effects of MCs in fish depend on the exposure concentrations, doses, time, and routes of exposure. Previous field and laboratory studies provided strong evidence of the associations between MC-induced immunotoxicity and fish death. In our review, we summarized that the immunotoxicity of MCs is primarily characterized by the inhibition of PP1 and PP2A, oxidative stress, immune cell damage, and inflammation, as well as apoptosis. The advances in fish immunoreaction upon encountering MCs will benefit the monitoring and prediction of fish health, helping to achieve an ecotoxicological goal and to ensure the sustainability of species. Future studies concerning MC-induced immunotoxicity should focus on adaptive immunity, the hormesis phenomenon and the synergistic effects of aquatic microbial pathogens.

Topics: Animals; Apoptosis; Fish Diseases; Fishes; Immunotoxins; Inflammation; Microcystins; Oxidative Stress; Protein Phosphatase 1; Protein Phosphatase 2

Cyanobacteria are present in all aquatic ecosystems throughout the world. They are able to produce toxic secondary metabolites, and microcystins are those most frequently found. Research has displayed a negative influence of microcystins and closely related nodularin on fish, and various histopathological alterations have been observed in many organs of the exposed fish. The aim of this article is to summarize the present knowledge of the impact of microcystins and nodularin on the histology of fish. The observed negative effects of cyanotoxins indicate that cyanobacteria and their toxins are a relevant medical (due to irritation, acute poisoning, tumor promotion, and carcinogenesis), ecotoxicological, and economic problem that may affect both fish and fish consumers including humans.

Topics: Animals; Carcinogenesis; Cyanobacteria; Fish Diseases; Microcystins; Peptides, Cyclic

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.

Topics: Animals; Fish Diseases; Microcystins; Salmo salar

Cyanobacterial blooms threaten human health as well as the population of other living organisms in the aquatic environment, particularly due to the production of natural toxic components, the cyanotoxin. So far, the most studied cyanotoxins are microcystins (MCs). In this study, the hepatic alterations at histological, proteome and transcriptome levels were evaluated in female and male medaka fish chronically exposed to 1 and 5 μg L

Topics: Animals; Bacterial Toxins; Cell Extracts; Chemical and Drug Induced Liver Injury; Circadian Rhythm; Down-Regulation; Female; Fish Diseases; Glycogen; Lipid Metabolism; Liver; Male; Microcystins; Microcystis; Oryzias; Oviparity; Protein Biosynthesis; Proteome; Reproduction; Transcriptome

Field and experimental studies were conducted to investigate pathological characterizations and biochemical responses in the liver and kidney of the phytoplanktivorous bighead carp after intraperitoneal (i.p.) administration of microcystins (MCs) and exposure to natural cyanobacterial blooms in Meiliang Bay, Lake Taihu. Bighead carp in field and laboratory studies showed a progressive recovery of structure and function in terms of histological, cellular, and biochemical features. In laboratory study, when fish were i.p. injected with extracted MCs at the doses of 200 and 500 microg MC-LReq/kg body weight, respectively, liver pathology in bighead carp was observed in a time dose-dependent manner within 24 h postinjection and characterized by disruption of liver structure, condensed cytoplasm, and the appearance of massive hepatocytes with karyopyknosis, karyorrhexis, and karyolysis. In comparison with previous studies on other fish, bighead carp in field study endured higher MC doses and longer-term exposure, but displayed less damage in the liver and kidney. Ultrastructural examination in the liver revealed the presence of lysosome proliferation, suggesting that bighead carp might eliminate or lessen cell damage caused by MCs through lysosome activation. Biochemically, sensitive responses in the antioxidant enzymes and higher basal glutathione concentrations might be responsible for their powerful resistance to MCs, suggesting that bighead carp can be used as biomanipulation fish to counteract cyanotoxin contamination.

Topics: Animals; Carps; Catalase; China; Fish Diseases; Fresh Water; Glutathione; Glutathione Peroxidase; Glutathione Transferase; Kidney; Liver; Microcystins; Microcystis; Microscopy, Electron, Transmission; Seasons; Superoxide Dismutase; Water Microbiology

Previous reports demonstrated that microcystin and related cyanobacteria polypeptides are rapidly cleared from plasma and accumulate in liver tissue. In the present study, we have used their ability to inhibit protein phosphatases to show that these cyanobacteria hepatotoxins are excreted into the bile of experimentally poisoned rainbow trout. At various times after oral administration of hepatotoxic Microcystis aeruginosa, bile samples were analysed for microcystin content by methanol extraction and protein phosphatase assays. An inhibitory principle that specifically suppressed protein phosphatase activity was detected in all bile samples removed between 1 and 72 h after oral exposure to toxic algae. These results indicate that biochemically active microcystin molecules are excreted into the biliary tract of poisoned fish.

Topics: Animals; Bacterial Toxins; Bile; Cyanobacteria; Enzyme Inhibitors; Fish Diseases; Liver Diseases; Microcystins; Oncorhynchus mykiss; Peptides, Cyclic; Phosphoprotein Phosphatases; Time Factors

Microcystin and related toxic peptides produced by cyanobacteria (blue-green algae) are potent and selective inhibitors of protein phosphatases 1 and 2A. We adapted existing enzymatic techniques to analyze the liver of rainbow trout after oral administration of hepatotoxic cyanobacteria. Liver tissue was removed 3 and 12 hours after treatment, and phosphatase activity was determined in liver extracts, using a specific phosphoprotein substrate. In all samples from fish exposed to toxic cyanobacteria, phosphatase activity was suppressed, whereas the control enzyme, lactate dehydrogenase, present in the same liver extract, was not affected by cyanobacteria. Thus, experimental poisoning by hepatotoxic cyanobacteria resulted in an abnormally low ratio of phosphatase to lactate dehydrogenase activity in the liver extracts. These results indicate that specific inhibition of phosphatases 1 and 2A may provide a useful diagnostic tool to determine the early effects of cyanobacteria toxic peptides directly in liver samples from poisoned animals. Although this test was developed with rainbow trout, it should be possible to extend the analysis of liver phosphatase activity to other species, including sheep and cattle, which are frequently affected by hepatotoxic cyanobacteria.

Topics: Animals; Bacterial Toxins; Cyanobacteria; Cyanobacteria Toxins; Enzyme Inhibitors; Fish Diseases; L-Lactate Dehydrogenase; Liver; Liver Diseases; Marine Toxins; Microcystins; Oncorhynchus mykiss; Peptides, Cyclic; Phosphoprotein Phosphatases