Pathophysiologic effects of a toxic peptide from Microcystis aeruginosa.

Abstract

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.

• Authors: W H Adams, R D Stoner, D G Adams, D N Slatkin, H W Siegelman
• Journal: Toxicon : official journal of the International Society on Toxinology (Toxicon) Vol. 23 Issue 3 Pg. 441-7 ( 1985) ISSN: 0041-0101 [Print] England
• PMID: 3927523 (Publication Type: Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Research Support, U.S. Gov't, P.H.S.)

Chemical References

• Bacterial Toxins
• Peptides
• Hydrocortisone

Topics

• Animals
• Bacterial Toxins (antagonists & inhibitors, toxicity)
• Carbon Tetrachloride Poisoning (physiopathology)
• Chemical and Drug Induced Liver Injury (etiology, physiopathology)
• Female
• Hydrocortisone (pharmacology)
• Lethal Dose 50
• Liver Function Tests
• Mice
• Microcystis (metabolism)
• Peptides (toxicity)