title: Binding of enterotoxin from Clostridium perfringens type A to liver cells in vivo and in vitro. The enterotoxin causes membrane leakage.
abstract: Enterotoxin from Clostridium perfringens was shown to retain its biological activity after labelling with 125I. When injected intravenously into mice and rats, most of the radioactivity in the organs was present in the form of intact toxin. Studies of the tissue distribution of labelled enterotoxin showed the largest amounts in the liver, where the activity reached a maximum 10--15 min after administration. The highest concentration per g tissue was found in liver and kidneys. The radioactivity was excreted in the urine as a mixture of intact labelled toxin and low molecular weight degradation products. In vitro studies with purified parenchymal liver cells showed rapid release of lactate dehydrogenase (LDH) during treatment with enterotoxin, thus indicating severe membrane damage.
mesh_terms: D000818:Animals; D002462:Cell Membrane / Q000378:metabolism / Q000382:microbiology / Q000473:pathology; D003016:Clostridium perfringens / Q000378:metabolism*; D004589:Electrophoresis, Disc; D004768:Enterotoxins / Q000008:administration & dosage / Q000097:blood / Q000378:metabolism*; D007275:Injections, Intravenous; D007413:Intestinal Mucosa / Q000378:metabolism; D007668:Kidney / Q000378:metabolism; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008099:Liver / Q000201:enzymology / Q000378:metabolism* / Q000473:pathology; D008168:Lung / Q000378:metabolism; D008297:Male; D051379:Mice; D009206:Myocardium / Q000378:metabolism; D051381:Rats; D013154:Spleen / Q000378:metabolism; D014018:Tissue Distribution
chemical_list: D004768:Enterotoxins; D007770:L-Lactate Dehydrogenase