ABSTRACT
Effect of monensin, intercalated in liposomes on the cytotoxicities of ricin, Pseudomonas exotoxin A and diphtheria toxin in phagocytic and non-phagocytic cells as well as in mice has been studied. Intercalation does not disturb the integrity of the liposomal bilayer and substantially enhances the cytotoxicities of ricin and Pseudomonas exotoxin A in both phagocytic and non-phagocytic cells while it has no effect on diphtheria toxin. The observed effect is highly dependent on the liposomal lipid composition as well as cell types. The potentiating ability of monensin in neutral vesicle is 2.2-fold higher than in negatively charged vesicles in non-phagocytic cells while no difference was observed in phagocytic cells. Incorporation of stearylamine in liposomes reduces the potentiating effect of monensin. Liposomal monensin has also been found to enhance the cytotoxicity of ricin in mouse in vivo in a dose-dependent manner and is maximal when ricin is injected within 60 min of monensin injection. Liposomal monensin remains in circulation for 2 hr while free monensin remains only for 15 min. Tissue distribution studies reveal that liposomal monensin is present mainly in the liver and spleen which are also the major sites for ricin accumulation. Thus liposome is found to be an effective delivery vehicle for monensin to potentiate the cytotoxicity of immunotoxins or hormonotoxins and could prove useful for selective elimination of cancer cells.
Subject(s)
ADP Ribose Transferases , Animals , Bacterial Toxins , CHO Cells , Cell Survival/drug effects , Cricetinae , Diphtheria Toxin/toxicity , Drug Carriers , Drug Synergism , Exotoxins/toxicity , Lipid Bilayers , Macrophages/cytology , Mice , Monensin/administration & dosage , Phagocytosis , Pseudomonas aeruginosa , Ricin/toxicity , Virulence FactorsABSTRACT
Säo abordados alguns fatores de virulência da Pseudomonas aeruginosa e seus efeitos sobre organismos celulares
Subject(s)
Pseudomonas aeruginosa/pathogenicity , Virulence , Exotoxins/toxicity , Pseudomonas Infections/pathology , Pancreatic Elastase/toxicity , Peptide Hydrolases/toxicity , Pseudomonas aeruginosa/enzymologyABSTRACT
Toxic chock syndrome is an acute febrile illness involving multiple organ systems. It was first described and associated with staphylococcus aureus since 1978. The clinical features are typically: abrupt onset, fever [39°C or greater], diffuse erythematous macula rash, shock and multiple organ dysfunction. We report a case of women; the usual clinical characteristics were found. T.S.S. has been associated with many infection by staphylococcus [vaginal, cutanuous and post-operative]. The syndrome is caused by the production, absorption and action of exotoxines. The treatment must correct organ dysfunction; antimicrobial therapy should be instituted. The mortality of the syndrom is less than 8%; the recurrence illness is possible but is very rare