Osmotic stabilizers differentially inhibit permeability alterations induced in Vero cells by Clostridium perfringens enterotoxin.
Using a sensitive Vero (African green monkey kidney) cell model system, studies were performed to further investigate whether Clostridium perfringens enterotoxin acts via disruption of the colloid-osmotic equilibrium of sensitive cells. Enterotoxin was shown to cause a rapid loss of intracellular 86Rb+ (Mr approx. 100) with time- and dose-dependent kinetics. The enterotoxin-induced release of intracellular 86Rb+ preceded the loss of two larger labels, 51Cr label (Mr approx. 3500) and 3H-labeled nucleotides (Mr less than 1000). The osmotic stabilizers, sucrose and poly(ethylene glycol), differentially inhibited enterotoxin-induced larger label loss versus 86Rb+ loss. Further, enterotoxin was shown to cause a rapid influx of 24Na+ that was not significantly inhibited by osmotic stabilizers. Additional studies demonstrated that lysosomotropic agents were not protective against characteristic enterotoxin-induced membrane permeability alterations or morphological damage. Taken collectively, these results are consistent with an action for enterotoxin which involves a disruption of the osmotic equilibrium.
D000818:Animals; D002460:Cell Line; D002462:Cell Membrane / Q000378:metabolism*; D002463:Cell Membrane Permeability / Q000187:drug effects*; D002522:Chlorocebus aethiops; D004768:Enterotoxins / Q000494:pharmacology*; D007668:Kidney; D009711:Nucleotides / Q000378:metabolism; D009995:Osmosis; D011092:Polyethylene Glycols / Q000494:pharmacology*; D011868:Radioisotopes; D012413:Rubidium / Q000378:metabolism; D012979:Sodium Radioisotopes / Q000378:metabolism; D013395:Sucrose / Q000494:pharmacology*
D004768:Enterotoxins; D009711:Nucleotides; D011868:Radioisotopes; D012979:Sodium Radioisotopes; C035598:enterotoxin, Clostridium; D011092:Polyethylene Glycols; D013395:Sucrose; D012413:Rubidium