Algae and some Cyanobacteria, being a core part of primary production, act as a food organism for many fishes and other aquatic organisms. But they can also be responsible for fish kill or illness. Review on Cyanobacteria effect on fish growth, survival, and recruitment is the need of the hour. The mechanisms of toxicity of cyanotoxins and their toxic metabolites in fish have been scarcely covered. The effects may be sublethal on growth, physiology, survival, recruitment, and in long run, it may have a role in the fish’s adaptive response to abiotic and other biotic stressors. Around 46 species from genera of Microcystis, Cylindrospermopsis, Synechococcus, Anabaena, Lyngbya, Oscillatoria, etc. have been shown to cause toxic effects in aquatic system. The bloom of these cyanobacteria is primarily associated with altered temperature and nutrient load in water bodies due to effluents from municipal discharge and aquaculture. Their acute or chronic toxic effects may vary depending on the species, type of toxin produced, and concentration. The various cyanotoxins are grouped as hepatotoxins like microcystin, nodularin cylindrospermopsin, neurotoxins; like anatoxins, homoanatoxins, dermatotoxins; like aplysiatoxin, debromoaplysiatoxins, lyngbyatoxins, and pyrogenic component; like lipopolysaccharides (LPS). The concentration of the specific cyanotoxin in the fish body and the water along with other factors such as the length of exposure, fish metabolic processes, water parameters like dissolved oxygen and temperature, are likely to impact cyanotoxin toxicity in freshwater fish. The impact of such toxicity may be reflected on the individual species level, ecosystem level, and even at the culture system level.

Keywords: cyanobacteria, cyanotoxins, aquatic system, fish physiology, toxicity, aquaculture

The term ‘algae’ is a diversified informal term for microscopically small, unicellular photosynthetic organisms which form colonies and are shown as minute green particles. These tend to distribute smoothly throughout the water and cause more turbidity with higher density. However, algae are the core part of primary production in the aquatic system and they act as a food organism for many fishes and food organisms, being in the food chain of fish. The algae have very good nutritional quality and they make a major part of phytoplanktonic biomass in a pond and other aquatic systems. But some of these algae have been known as causing death or illness in cultures fishes and as well as different aquatic mammals, birds, etc. through, the toxicity of Cyanophyta. Cyanophyta or Cyanobacteria are nothing but a mixture of bacteria and some of the algae which contain blue-green (c-phycocyanin) and green pigments (chlorophyll- a), carotenes, xanthophylls, and a red pigment (c- phycoerythrin) that can execute photosynthesis.

The toxic effect of the cyanophyta is one of the major concerns for humans and other animals. However, its effect on fishes, their growth and survival, recruitment is the need of the hour especially in the present condition of anthropogenic activity leading to community change in the aquatic system and natural ponds.

Most of the papers were published based on toxic freshwater algae and Prescott¹ reported that toxicity of algae has tended to kill fish. Similarly, Olson² published a brief summary of poisonous plankton, and Scott³ presented a general paper on fresh-water algal poisons. So, the theories of most of the studies are based on human activities (agriculture runoff, sewage treatment, chemical fertilization, etc.) which led to an unrestricted proliferation of algae due enrichment of water in nutrients. Proliferation is a consequence of eutrophication). The Cyanobacteria of freshwater bodies are very common to cause bloom and show a huge impact upon recreational and culture water bodies.

In temperate regions, cyano bacterial dominance is most pronounced during the summer months. But in tropical climates, spring and post-monsoon seasons are the actual time of eutrophication of such blooms. The cyano bacterial toxins are the most studied algal toxin in the freshwater system. The understanding of the mechanisms of toxicity of cyanotoxins and their toxic metabolites from algae in fish has been rarely covered.

Similarly, marine species of various genera often contain toxins and are responsible for toxic bloom in coastal water leading to fish kills. So, it is reasonable to expect toxic species among these groups in freshwater aquatic systems like lakes, chaurs (shallow water bodies in wetlands), ponds, and other aquaculture systems. We can say this review may focus primarily on the freshwater fish health impacts of cyanobacteria, while many species of freshwater algae grow rapidly in eutrophic waters, the toxin does not accumulate which is hazardous to the health of livestock.⁴ When we understand the toxic effect, it may be a sublethal impact like, on growth, physiology, survival, and recruitment in long run, which may have a role on the adaptation of the fish in response to abiotic and other biotic stressors. The toxic effect and sub lethal levels are something of great concern as it may have role in growth reduction and a stress inducing factor for cultured fish. Therefore on farm several chemical like Cupper sulphate, hydrogen peroxide etc. have been used and evaluated.⁵ Similar study by Kang et al., reflects such initiatives.^6,7

Cyanobacteria can be benthic or pelagic, and their form makes them one of the most varied bacterial phyla. Cyanobacteria have been discovered classified into five distinct morphological parts, including unicellular colonies with binary fission, uni-colonies having numerous fissions, multicellular colonies, differentiated cells in multicellular colonies, and branching colonies clusters of developed cells that are multicellular in nature.⁸

The cyano bacterial colonies are large enough to be seen from the naked eye. When they are in abundant amount and form bloom, it alters the colour of water and sometimes they form thick scum on the surface of the water. Consumption of fish from such waters is an important route of human exposure to cyanotoxins.⁹ As much as 40% of global finfish production comes from freshwater,¹⁰ and cyanotoxins have been detected in freshwater fish from around the world.¹¹ However, the accumulated toxins give an impact on other animals eating the fish, but fishes are the first target of such toxins. There is enough chance of toxic effect on fish and other aquatic communities, when these toxic compounds or their metabolites leach to water.

At least 46 species (approx. 60% of cyano bacterial samples) have been shown to cause toxic effects in vertebrates.¹² The most common toxic cyanobacteria in fresh water are Microcystis spp., Cylindrospermopsis raciborskii, Planktothrix (syn. Oscillatoria) rubescens, Synechococcuss, Anabaena spp., some Oscillatoria spp. etc. Anabaena, Aphanizomenon, Oscillatoria, and Microcystis grow best at temperatures ranging from 25 °C to 35 °C. The bloom of cyanobacteria is primarily associated with altered temperature, nutrient load in water bodies due to effluents from municipal discharge and aquaculture. Secchi disc transparency in fish ponds provides a rough estimate of plankton abundance. The most important factor influencing pond productivity is dissolved oxygen.

Microcystins and neurotoxins are the most common cyano bacterial poisons or cyanotoxins. There are dangerous and harmful strains in most species, however, nontoxic strains do exist. Microcystins is produced by Microcystis, the most common bloom-forming genus,¹³ is virtually always harmful in the wild as their blooms resemble a greenish, thick, paint-like (sometimes granular) material that accumulates along shores of ponds or lakes. While the conditions that contribute to cyanobacteria proliferation are well established,⁴ and varies widely. The factors that lead to harmful strain dominance are the favourable circumstances, such as high temperature, strong light, and pH, and increased nutrient availability. The cyanobacteria can proliferate swiftly in such surface waters and create blooms.¹⁴

Because certain cyano bacterial species create extremely poisonous secondary metabolites known as cyanotoxins so these blooms can be dangerous to people, other animals, and aquatic life. Blooms can persist anywhere from a few days to several months. They have grown in size and frequency in most locations, and are typically caused by an excess of nutrients in the environment. The water contains the two most prevalent macronutrients, which are nitrogen and phosphorus, and their fixation from agricultural and industrial sources, low circulation and other variables have a major role like increased water temperature.¹⁵ Hazardous cyano bacterial species may benefit from global climate change. As they can tolerate adverse climatic condition and boost their growth rate, dominance, persistence, geographical dispersion, and activity.^16,17

Toxins produced by some cyanobacteria species or strains may threaten aquatic life or fish. The probable acute toxic effect¹⁸ of cyanotoxins may be among a few of following: decreased survival and reduced growth; reduced swimming motions or activity; lethargy and gasping; full paralysis; gastroenteritis; hepatotoxicity and hepatic oxidative stress; hyperplasia and histopathological damage to vital organs. Similarly, chronic impacts may be witnessed on the population or community level, are: lower fertility and population growth rate; poor recruitment performance; reduce biological growth potential; reduced reproductive performance; change in community structure of the aquatic ecosystem; altered species or trophic dominance. These effects can also occur as a result of sub-lethal doses. Effects, on the other hand, vary depending on the species, type of toxin produced, and concentration.¹⁹

The bloom occurs in aquaculture system and their load in water produce scum. The vertical movement of these algae is triggered by buoyancy regulation via intracellular gas vesicles in several species. Changing the amount of gas in the vesicles to regulate buoyancy is a slow process. They are driven to leeward side by light breezes, where they produce scums.

In extreme circumstances, these agglomerations can become extremely dense and even gelatinous.⁴ Dying and lysing cells (i.e., cell rapture) release their toxins into the water, where pigments can take on a coppery hue. Wave motion can swiftly break scums and re-disperse them with new wind mixing. However, scum material may take a long time to disperse, especially in shallow bays or ponds, due to either wave wash or cell disintegration. However, Cyanobacteria mats, also known as benthic mats, are typically caused by planktonic species living in eutrophic waters (which are relatively low in plant nutrients), but they can also be caused by pollution and a lack of oxygen. During sunny days, their photosynthesis may result in high rates of oxygen production, forming bubbles that loosen and drive parts of the mats to the surface. Beach mats of benthic cyanobacteria washed to the shore and scavenged by dogs have been lethal²⁰ and cyanobacteria may also be responsible for cattle deaths on Swiss alpine meadows.²¹A similar kind of threat is for aquatic species as a target or non-target species.

However, it is essential to have knowledge on the potential toxicity of such mats in aquatic systems especially associated with aquaculture practice or nearby areas. Toxic blooms may reappear periodically in aquaculture environments, and fishes under culture may be chronically exposed to cyanotoxins at relatively low doses. The concentration of the specific cyanotoxins in the body and the water, as well as the length of exposure and fish metabolic processes, water parameters like temperature, are likely to impact cyanotoxin concentrations in freshwater fish.²² The impact of such toxicity may be reflected on the individual species level, ecosystem-level, and even at system level in particular aquaculture system.

Microcystins are cyclic heptapeptides that are commonly produced by different cyano bacterial genera those are discussed earlier. They are also called hepatotoxin, named from the fact that the liver is their principal target (Table 1). In most places, anthropogenic nutrient over-enrichment (eutrophication), as well as other variables such as intense agriculture growth, fast industrialization, and urbanization, appears to increase the incidence of microcystins-producing HABs.

Microcystins, nodular in, and cylindrospermopsins are examples of known toxins that can induce liver and kidney damage, as well as cytotoxicity, neurotoxicity, skin toxicity, gastrointestinal disorders, and other issues. These effects may arise immediately after exposure or may take days to manifest. Among them Microcystin-LR is the most toxic, well studied and abundant variant and is one of the most important algal toxins that has received worldwide attention. Microcystin poisoning has different clinical symptoms depending on the method of exposure, the quantity of exposure, and the combination of components involved in the exposure. In most exposures, low to moderate levels of exposure of mammals to toxic blooms are linked to irritating effects in the skin, respiratory system, and gastrointestinal system, leading to inflammatory reactions. Higher amounts of exposure, particularly oral exposures cause liver damage, and if the liver damage is severe, it can be fatal.²³

Liver edema and elevated concentrations of liver enzymes like alanine aminotransferase and aspartate aminotransferase in the blood are the first indicators of liver injury. Inappetence, sadness, and vomiting are common early symptoms, followed by diarrhoea that can become severe and haemorrhagic within minutes to hours of contact. Inappetence and sadness get worse with time. Recumbency and coma may be connected with the latter stages of fatal poisoning.²⁴ Microcystin-LR has the potential to release carcinogens to the human’s liver, testes after consuming toxin affected fishes.²⁵ It can progress colorectal carcinoma²⁶ It can also stimulate epithelial-mesenchymal transitions (EMT), which regulate cancer cell’s motility and invasive properties that can lead to metastasis in embryonic development and cancer progression.²⁷ Such symptoms of toxicity mostly based on freshwater system-based toxicity are directly linked to humans. However, such impact may have on fishes and is a matter of widespread study and delineation in species-specific manner.

Microcystin exposure causes cellular damage in fish, notably liver damage, comparable to the consequences reported in mammals²⁸ When compared to young fish, mature fish are more resistant to microcystin toxicosis. Although fish have the capacity to avoid areas of toxic algal growth, sublethal liver injury in fish is connected with microcystin accumulation in fish food items. Mussels, snails, and zoo plankton.²⁹ Fish are equally vulnerable to low oxygen levels during such bloom.

Water oxygen demand is induced by algal bloom respiration as well as with algal degradation of scum, and this impact may potentially contribute to fish fatalities³⁰ The impact of lower and greater doses of microcystin-LR has been reflected at cellular or tissue level in form of apoptosis and necrosis in lymphocytes, reorganization of the actin cytoskeleton, cell shrinkage, and the absence of filopodia were also detected in phagocytes, and finally the immune system dysfunction.³¹ Kozdeba et al.³² reported that microcystin irritated the skin after epidermal exposure and in situations of skin injury, quicker penetration to deeper cell layers and absorption into the systemic circulation might be predicted. Additionally, only after lengthier skin exposures, the persistent harmful effects such as keratinocyte migration and cytoskeleton were observed.

Histopathological examinations of fish killed during cyano bacterial blooms revealed that the cause of death was mostly related to gill, digestive system, and liver damage. The gill injury was most likely caused by the high pH created by cyano bacterial photosynthetic activity before to bloom collapse. Increased microcystin intake may have led to liver necrosis. Other pathological symptoms associated with toxic blooms include liver, heart, kidney, skin, gills, and spleen damage¹² Malbrouck and Kestemont²⁹ reported the occurrence of disturbances in the main development processes can often result in death. Fish in the early stages of life are more sensitive to toxic compounds than adults and juveniles, probably due to their thin epithelial layer combined with a relatively large body surface area or the limited ability of the metabolic process to neutralize the cyanotoxins. Liu et al.³³ observed that mortality in juvenile loach (Misgurunsmizolepis) was dependent on the developmental stage of loach embryos. Similarly, the toxicity of different cyano bacterial blooms on the embryo and larval development of carp Cyprinus carpio were investigated. Microcystis spp. was found to dominate in two samples. Both the samples of complex cyano bacterial biomass, in that the aqueous extracts, showed embryo toxic effects such as significant fish mortality and delayed hatching. According to their findings, the individual carp exposed to higher concentrations of some fractions from all biomasses showed missing eye pigmentation and incomplete filling of the air bladder after 120 hours.

Tencalla et al.³⁴ studied the effects of MC-LR on yearling rainbow trout where microcystins travel primarily through the gastrointestinal tract by force-feeding in trout, and that toxicity manifests as massive hepatic necrosis followed by fish deaths, whereas immersion of adults and juveniles in contaminated water did not cause toxic effects. M. aeruginosa concentrations of 8-16 mg freeze-dried algae/L were not found to be toxic to trout when added to water. When 1.440 mg of lyophilized algae/kg of body weight was passed through the gills for 18 hours, the trout died within 96 hours. Oberemm et al.³⁵ discovered that exposure to concentrations of 50 and 5 mg/L MC-LR reduced embryonic survival rates by 40% and 20%, respectively, as well as growth and weight by 25%, in a study on the effects of microcystins in Danio rerio. Other evidence suggests that sensitivity differences while exposure of toxins between species can be significant: goldfish were found to be nearly 30 times less susceptible to i.p. microcystin than mice.³⁶

The gill damage was most likely caused by the high pH caused by cyano bacterial photosynthesis activity prior to bloom collapse, as well as the higher level of ammonia caused by cyano bacterial decomposition (Table 2). However, gill damage may have increased microcystin uptake, leading to liver necrosis. Dissolved microcystin-LR has been shown in Tilapia and trout to cause gill damage.³⁷

ERodger et al.³⁸ and Rabergh et al.³⁹ conducted experiments on trout and carp, respectively. The latter study focused on degenerative changes in the kidney tubules and glomeruli. Carbis et al.⁴⁰ described the effect of microcystins on Cyprinus carpio, in natural field conditions in Australia as hepatocyte atrophy, gills with pinpoint necrosis, epithelial ballooning, folded lamellar tips, and exfoliation of the lamellar epithelium, elevated aspartate amino transferase activity, and serum bilirubin concentrations. Laboratory studies show that dissolved microcystins can affect fish embryos and behaviour. ^41,42 Anatoxins also caused behavioural changes in juvenile Cyprinus carpio, such as rapid opercular movement and abnormal swimming, and lateral malformations and increased mortality in Danio rerio embryos.⁴³ Such physiological impact has been reported in fishes and been found to be quite wide spread. Therefore it creates concern wide aspect.

Cyanobacteria are vital in a variety of habitats, but when conditions are good, they may dominate aquatic environments and multiply excessively. Human activities are mostly to blame for the abundant supply of nutrients in bodies of water, which contributes to the increased severity of cyano bacterial blooms. Cyanotoxins cause serious poisoning in aquatic species and humans. Ingestion of Microcystis cells has negative consequences in a variety of aquatic species. In the case of fish, the toxic effects induced disruptions in the primary development processes, making the early life stages more vulnerable to microcystin. Anatoxins also caused behavioural changes in young C. carpio, such as fast opercular movement and aberrant swimming. Saxitoxins caused lateral abnormalities in D. rerio embryos and increased mortality. Due to these toxic impacts the concern of cyanophyta and its control in aquaculture is gaining very much importance. Effort in this regard has been made through several studies like Buley et al. ⁴⁴  investigated different product to control the bloom in aquaculture. Similarly Drummond et al.^45,46  studied other strategies to control the cyano bacterial blooms in reservoirs. However, given the great potential of cyanobacteria for the production of compounds important in the discovery of new medicines, there is also a need for additional efforts to identify biomolecules, develop new methods to isolate cyano bacterial toxins, and conduct new research on anticancer compounds obtained from cyanobacteria.

We put my thanks and gratitude to the Director ICAR - CIFE Mumbai for time-to-time support and facility.

We declare that there is no conflict of interest among the authors or with any one related to the present work.

1. Prescott GW. Some effects of the blue-green algae, Aphanizomenon flos- aquae, on lake fish. Collect Net. 1933;8(4):77.
2. Olson TA. History of toxic plankton and associated phenomena. Sewage Works Eng. 1949;20(2).
3. Scott RM. Algal toxins. Public Works. 1952;54–55:65–66.
4. Chorus I, Bartram J. Toxic cyanobacteria in water. A guide to their public health consequences, monitoring and management. E & FN Spon on behalf of the World Health Organization. 1999.
5. Huang IS, Zimba PV. Hydrogen peroxide, an ecofriendly remediation method for controlling Microcystis aeruginosa toxic blooms. J Appl Phycol. 2020;32(5):3133–3142
6. Li K, Mucci M, Fang J. et al. New is not always better: Toxicity of novel copper based algaecides to Daphnia magna. Ecotoxicol Environ Safety. 2022;241:113817.
7. Kang L, Mucci M, Lürling M. Influence of temperature and pH on phosphate removal efficiency of different sorbents used in lake restoration. Sci Total Environ. 2022;812:151489
8. Schirrmeister BE, Antonelli A, Bagheri HC. The origin of multicellularity in cyanobacteria. BMC Evol Biol. 2011;11(1):45.
9. Poste AE, Hecky RE, Guildford SJ. Evaluating microcystin exposure risk through fish consumption. Environ Sci Technol. 2011;45(13):5806–5811.
10. Lynch AJ, Cooke SJ, Deines AM, et al. The social, economic, and environmental importance of inland fish and fisheries. Environ Rev. 2016;24(2):115–121.
11. Lee J, Lee S, Jiang X. Cyanobacterial toxins in freshwater and food: important sources of exposure to humans. Annu Rev Food Sci Technol. 2017;8:281–304.
12. Sivonen K, Jones J. Cyanobacterial toxins. In: Chorus I, Bartram J. Toxic cyanobacteria in water. A guide to their public health consequences, monitoring and management. Published by E & FN Spon on behalf of the World Health Organization. 1999;41–112.
13. Carmichael W. Toxic Microcystis and the environment. In: Watanabe M, Harada K, Carmichael W, Fujiki H, ed. Toxic Microcystis. Boca Raton, FL, CRC Press. 1995;1–12.
14. Dantas ÊW, Moura AN, Bittencourt-Oliveira MDC. Cyanobacterial blooms in stratified and destratified eutrophic reservoirs in semi-arid region of Brazil. An Acad Bras Ciênc. 2011;83:1327–1338.
15. Van der Merwe, Deon. Handbook of Toxicology of Chemical Warfare Agents Cyanobacterial (Blue-Green Algae) Toxins. 2015;421–429.
16. Paerl HW, Huisman J. Climate change: a catalyst for global expansion of harmful cyano bacterial blooms. Environ Microbiol Rep. 2009;1(1):27–37.
17. Bláha L, Babica P, Maršálek B. Toxins produced in cyanobacterial water blooms–toxicity and risks. Interdiscip Toxicol. 2009;2(2):36–41.
18. Landsberg JH. The effects of harmful algal blooms on aquatic organisms. Reviews in Fisheries Science. 2002;10(2):113–390.
19. Billoir E, Ferrão-Filho AS, Delignette-Muller ML, et al. DEBtox theory and matrix population models as helpful tools in understanding the interaction between toxic cyanobacteria and zooplankton. J Theor Biol. 2009;258(3):380–388.
20. Edwards C, Beattie K, Scrimgeour C, et al. Identification of anatoxin-A in benthic cyanobacteria (blue-green algae) and in associated dog poisonings at Loch Insh, Scotland. Toxicon. 1992;30(10):1165–1167.
21. Mez K, Hanselmann K, Preisig HR. Environmental conditions in high mountain lakes containing toxic benthic cyanobacteria. Hydrobiologia. 1998;368:1–16.
22. Gurbuz F, Uzunmehmetoğlu OY, Diler Ö, et al. Occurrence of microcystins in water, bloom, sediment and fish from a public water supply. Sci Total Environ. 2016;562:860–868.
23. Briand JF, Jacquet S, Bernard C, et al. Health hazards for terrestrial vertebrates from toxic cyanobacteria in surface water ecosystems. Vet Res. 2003;34(4):361–377.
24. Kaur G. Freshwater Cyanotoxins. Biomarkers in Toxicology. Academic Press. 2019;601–613.
25. Lone Y, Koiri RK, Bhide M. An overview of the toxic effect of potential human carcinogen Microcystin-LR on testis. Toxicol Rep. 2015;2:289–296.
26. Miao C, Ren Y, Chen M, et al. Microcystin-LR promotes migration and invasion of colorectal cancer through matrix metalloproteinase-13 up-regulation. Mol Carcinog. 2016;55(5):514–524.
27. Ren Y, Yang M, Chen M, et al. Microcystin-LR promotes epithelial-mesenchymal transition in colorectal cancer cells through PI3-K/AKT and SMAD2. Toxicol Lett. 2017;265:53–60.
28. Tencalla F, Dietrich D. Biochemical characterization of microcystin toxicity in rainbow trout (Oncorhynchus mykiss). Toxicon. 1997;35(4):583–595.
29. Malbrouck C, Kestemont P. Effects of microcystins on fish. Environ Toxicol Chem. 2006;25(1):72–86.
30. Ibelings BW, Havens KE. Cyanobacterial toxins: a qualitative meta–analysis of concentrations, dosage and effects in freshwater, estuarine and marine biota. Adv Exp Med Biol. 2008;619:675–732.
31. Rymuszka A, Adaszek Ł. Cytotoxic effects and changes in cytokine gene expression induced by microcystin-containing extract in fish immune cells–An in vitro and in vivo study. Fish Shellfish Immunol. 2013;34(6):1524–1532.
32. Kozdęba M, Borowczyk J, Zimoląg E, et al. Microcystin-LR affects properties of human epidermal skin cells crucial for regenerative processes. Toxicon. 2014;80:38–46.
33. Liu Y, Song L, Li X, et al. The toxic effects of microcystin-LR on embryo-larval and juvenile development of loach, Misguruns mizolepis Gunthe. Toxicon. 2002;40(4):395–399.
34. Tencalla FG, Dietrich DR, Schlatter C. Toxicity of Microcystis aeruginosa peptide toxin to yearling rainbow trout (Oncorhynchus mykiss). Aquatic Toxicology. 1994;30(3):215–224.
35. Oberemm A, Becker J, Codd GA, et al. Effects of cyano bacterial toxins and aqueous crude extracts of cyanobacteria on the development of fish and amphibians. Environmen Toxicol. 1999;14(1):77–88.
36. Sugaya Y, Yasuno M, Yani T. Effects of toxic Microcystis viridis and isolated toxins on goldfish. Japan J Limnol. 1990;51(3):149–153.
37. Bury NR, Flik G, Eddy FB, et al. The effects of cyanobacteria and the cyano bacterial toxin microcystin-LR on Ca2+ transport and Na+ /K+ - ATPase in Tilapia gills. J Exp Biol. 1996;199:1319–1326.
38. Rodger HD, Turnbull T, Edwards C, et al. Cyano bacterial bloom associated pathology in brown trout Salmo trutta L. in Loch Leven, Scotland. J Fish Dis. 1994;17:177–181.
39. Rabergh CMI, Bylund G, Eriksson JE. Histopathological effect of microcystin LR a cyclic polypeptide from the cyano bacterium Microcystis aeruginosa on common carp (Cyprinus carpio L). Aquat Tox. 1991;20:131–146.
40. Carbis CR, Rawlin GT, Grant P, et al. A study of feral carp Cyprinus carpio L, exposed to Microcystis aeruginosa at Lake Mokoan, Australia, and possible implication on fish health. J Fish Diseases. 1997;20:81–91.
41. Oberemm A, Fastner J, Steinberg C. Effects of MC-LR and cyanobacterial crude extracts on embryo-larval development of zebrafish. Water Res. 1997;31(11):2918–2921.
42. Baganz D, Staaks G, Steinberg C. Impact of the cyanobacteria toxin, microcystin-LR, on the behavior of zebrafish, Danio rerio. Water Res. 1998;32(3):948–952.
43. Rodríguez V, Moura S, Pinto E, et al. Toxicological and chemical aspects of Anatoxin-a and its analogues. Chem New. 2006;29:1365–1371.
44. Buley RP, Adams C, Belfiore AP, et al. Field evaluation of seven products to control cyano bacterial blooms in aquaculture. Environ Sci Pollut Res Int. 2021;28(23):29971–29983.
45. Drummond E, Leite VBG, Noyma NP, et al. Temporal and spatial variation in the efficiency of a Floc & Sink technique for controlling cyanobacterial blooms in a tropical reservoir. Harmful Algae. 2022;117:102262.
46. Palíková M, Krejčí R, Hilscherová K, et al. Effect of different cyanobacterial biomasses and their fractions with variable microcystin content on embryonal development of carp (Cyprinus carpio L.). Aquat Toxicol. 2007;81(3):312–318.