cyanoginosin-lr and Hemorrhage

This study evaluated the effects of [D-Leu(1)]Microcystin-LR variants, by the exposure of Hypophthalmichthys molitrix to Microcystis aeruginosa NPLJ4. Fish was placed in aquariums and exposed to 10(5) cells mL(-1). For 15 days, 05 individuals were removed every 05 days, and tissue samples of liver, skeletal muscle and intestinal tract were collected for histopathologic analyses. Following exposure, those surviving were placed in clean water for 15 days to evaluate their recovery. A control without toxins was maintained in the same conditions and exhibited normal histology and no tissue damage. In exposed fish, samples were characterized by serious damages that similarly affected the different organs, such as dissociation of cells, necrosis and haemorrhage. Samples showed signs of recovery but severe damages were still observed. The results should be valuable to analyze the potency of microcystin toxicity and to help in the diagnosis of fish deaths.

Topics: Animals; Chemical and Drug Induced Liver Injury; Chromatography, High Pressure Liquid; Cyprinidae; Digestive System; Hemorrhage; Intestinal Diseases; Liver; Marine Toxins; Mass Spectrometry; Microcystins; Muscle, Skeletal; Muscular Diseases; Necrosis; Survival

In 26 hr laboratory trials a dose of 1000 micrograms/kg microcystin-LR (MC-LR) caused 100% mortality in rainbow trout, while no mortality was observed at doses of 400 micrograms/kg or less. The liver to body mass ratio increased in fish exposed to the toxin which was likely due to water retention in the liver. In contrast to mammalian studies, hemorrhage of the liver was rare in fish. Exposure to MC-LR caused widespread hepatocellular swelling and lysis of hepatocyte plasma membranes, resulting in liquifactive necrosis (organelles floating in a milieux of cellular debris). Kidney lesions in the fish consisted of coagulative tubular necrosis with a dilation of Bowman's space. Lesions observed in the liver and kidney of fish exposed to MC-LR were considerably different than those previously reported for mammals.

Topics: Animals; Bacterial Toxins; Body Weight; Dose-Response Relationship, Drug; Hemorrhage; Injections, Intraperitoneal; Kidney Tubules; Liver; Marine Toxins; Microcystins; Microscopy, Electron; Oncorhynchus mykiss; Organ Size; Peptides, Cyclic; Poisoning

Male rats were intraperitoneally administered a lethal dose of microcystin-LR (a toxin of cyanobacteria). Prior to haemorrhage in the liver, blood coagulation and platelet aggregation activities were measured. The number of cellular components, white blood cells, red blood cells and, especially, platelets, decreased 1-1.5 hr after the injection. Plasma kaolin-activated partial thromboplastin time was prolonged and fibrinogen concentration was reduced, but antithrombin III activity and fibrin degradation product concentration were not significantly changed. Platelet aggregation was not affected for up to 0.5-1.0 hr after administration. Sequential analyses of those parameters and hepatotoxic markers indicate that those hematologic changes as well as the hepatic injury occur suddenly after the massive bleeding. These results suggest that microcystin-LR does not directly act on the haemostatic system to cause a disseminated intravascular coagulation-like state. The decrease in blood coagulation activity and platelet particle concentration may be the results of secondary consumptive effects following the hepatic haemorrhage.

Topics: Animals; Bacterial Toxins; Blood Coagulation; Chemical and Drug Induced Liver Injury; Cyanobacteria; Disseminated Intravascular Coagulation; Fibrinogen; Hemorrhage; Liver; Liver Function Tests; Male; Marine Toxins; Microcystins; Partial Thromboplastin Time; Peptides, Cyclic; Phosphoprotein Phosphatases; Platelet Aggregation; Rats; Rats, Sprague-Dawley