Pathophysiologic effects of a toxic peptide from Microcystis aeruginosa.
Toxin-LR, a hexapeptide produced by Microcystis aeruginosa, causes marked hepatic vascular congestion, thrombocytopenia, microscopic pulmonary thrombi and death in 50-70 min when injected into mice. Although it is considered an hepatotoxin, we report that sublethal hepatocellular damage produced by CCl4 given 24 hr prior to toxin-LR administration prevents the acute deaths. However, CCl4-treated mice surviving toxin-LR acute effects often died during the subsequent three days. Pretreatment of mice with the microsomal enzyme inhibitors SKF 525A or cobaltous chloride did not alter the acute lethality of toxin-LR, but pharmacologic doses of hydrocortisone prevented both the acute and delayed deaths. X irradiation-induced thrombocytopenia or thrombocytopenia and leukopenia did not significantly affect the toxin's lethality. In vitro platelet aggregation or lysis did not occur during incubation with toxin-LR, nor was a humoral aggregating factor detected in plasma from toxin-injected mice.
D000818:Animals; D001427:Bacterial Toxins / Q000037:antagonists & inhibitors / Q000633:toxicity*; D002252:Carbon Tetrachloride Poisoning / Q000503:physiopathology; D056486:Chemical and Drug Induced Liver Injury / Q000209:etiology* / Q000503:physiopathology; D005260:Female; D006854:Hydrocortisone / Q000494:pharmacology; D007928:Lethal Dose 50; D008111:Liver Function Tests; D051379:Mice; D046931:Microcystis / Q000378:metabolism*; D010455:Peptides / Q000633:toxicity*
D001427:Bacterial Toxins; D010455:Peptides; D006854:Hydrocortisone