The effects of Clostridium perfringens enterotoxin on intracellular levels or transport of uridine, thymidine and leucine do not fully explain enterotoxin-induced inhibition of macromolecular synthesis in Vero cells.
Clostridium perfringens type A enterotoxin (CPE) has been shown previously to inhibit the incorporation of radiolabeled precursors into acid-insoluble material but the mechanism of inhibition is unknown. It has also been shown that extracellular calcium is required for some CPE effects. In this report, it is shown that CPE completely and virtually simultaneously inhibits incorporation of precursors into RNA, DNA and protein in either the presence or absence of extracellular divalent cations and that changes in intracellular precursor levels did not consistently correlate with this CPE-induced inhibition of incorporation. These results strongly suggest that CPE can inhibit macromolecular synthesis, not just inhibit precursor transport. It is inferred from this that CPE can affect DNA and RNA synthesis, and possibly protein synthesis, by altering other cellular processes besides, or in addition to, precursor transport and these effects then lead to a shutdown of macromolecular synthesis.
Hulkower
K I
KI
Department of Microbiology, Biochemistry and Molecular Biology, University of Pittsburgh School of Medicine, PA 15261.
McClane
B A
BA
D000818:Animals; D001692:Biological Transport / Q000187:drug effects; D002118:Calcium / Q000502:physiology; D004768:Enterotoxins / Q000494:pharmacology*; D007930:Leucine / Q000378:metabolism*; D009696:Nucleic Acids / Q000096:biosynthesis*; D014176:Protein Biosynthesis; D013936:Thymidine / Q000378:metabolism*; D014529:Uridine / Q000378:metabolism*; D014709:Vero Cells
D004768:Enterotoxins; D009696:Nucleic Acids; C035598:enterotoxin, Clostridium; D007930:Leucine; D002118:Calcium; D013936:Thymidine; D014529:Uridine