Crude extract of cyanobacteria (Radiocystis fernandoi, strain R28) induces liver impairments in fish

• Published in: Aquatic toxicology 2017-01, Vol.182, p.91-101
• Main Authors: Paulino, M.G., Tavares, D., Bieczynski, F., Pedrão, P.G., Souza, N.E.S., Sakuragui, M.M., Luquet, C.M., Terezan, A.P., Fernandes, J.B., Giani, A., Fernandes, M.N.
• Format: Article
• Language: English
• Subjects: Animals; Cyanobacteria - chemistry; Enzyme Activation - drug effects; Fishes - physiology; Hepatocytes - drug effects; Hoplias malabaricus; Liver - drug effects; Liver - enzymology; Liver - metabolism; Liver ultrastructure; Microcystin accumulation; Microcystins - metabolism; Microcystins - toxicity; Muscle; Muscle, Skeletal - drug effects; Muscle, Skeletal - metabolism; PP1 and PP2A activity; Protein Phosphatase 2 - metabolism; Water Pollutants, Chemical - toxicity
• ISSN: 0166-445X; 1879-1514
• DOI: 10.1016/j.aquatox.2016.11.012

•Radiocystis fernandoi strain R28 contains mainly microcystins RR and YR.•YR accumulated in liver after acute, and RR and YR after subchronic exposure.•Crude extract inhibited endogenous PP2A after subchronic exposure.•Crude extract induces structural and ultrastructural changes the liver.•Collagen fibers occupy great area of liver after subchronic exposure. Radiocystis fernandoi R28 strain is a cyanobacterium which produces mostly the RR and YR microcystin variants (MC-RR and MC-YR, respectively). The effects of crude extract of the R. fernandoi strain R28 were evaluated on the protein phosphatases and on the structure and ultrastructure of the liver of the Neotropical fish, Hoplias malabaricus, after acute and subchronic exposure. Concomitantly, the accumulation of the majority of MCs was determined in the liver and muscle. The fish were exposed to 120.60 MC-RR+MC-LR kg-fish−1 (=100μg MC-LReq kg-fish−1) for 12 and 96h (one single dose, acute exposure) and 30days (one similar dose every 72h, subchronic exposure). MCs did not accumulate in the muscle but, in the liver, MC-YR accumulated after acute exposure and MC-RR and MC-YR accumulation occurred after subchronic exposure. Protein phosphatase 2A (PP2A) activity was inhibited only after subchronic exposure. Acute exposure induced liver hyperemia, hemorrhage, changes in hepatocytes and cord-like disorganization. At the ultrastructural level, the decreasing of glycogen and lipid levels, the swelling of mitochondria and whirling of endoplasmic reticulum suggested hepatocyte necrosis. Subchronic exposure resulted in a complete disarrangement of cord-like hepatocytes, some recovery of mitochondria and whirling endoplasmic reticulum and extensive connective tissues containing fibrous materials in the liver parenchyma. Despite microcystin toxicity and liver alterations, no tumor was induced by MCs. In conclusion, the increased algal mass of R. fernandoi in tropical freshwater, producing mainly MC-RR and MC-YR variants, results in fish liver impairments.