Differentiation of HL-60 cells is promoted by H-toxin of Clostridium septicum

FEBS Lett. 1994 Sep 12;351(3):317-20. doi: 10.1016/0014-5793(94)00856-6.


H-toxin of Clostridium septicum potentiated dimethyl sulfoxide (DMSO)-induced differentiation of human promyelocytic leukemia HL-60 cells which were monitored by nuclear morphology and production of oxidative radicals. But, H-toxin did not induce differentiation of HL-60 cells in the absence of DMSO. These phenomena were not observed by staphylococcal leukocidin, a cytotoxin affecting to HL-60 cells. In HL-60 cells, ADP-ribosylation of 118, 93, 75 and 58 kDa membrane proteins was observed, but the ADP-ribosylation was not detected either in differentiated HL-60 cells by DMSO or in normal polymorphonuclear leukocytes of human. When the membranes of HL-60 cells were incubated with H-toxin, ADP-ribosylation of the membrane proteins was inhibited. Such suppressive effects on ADP-ribosylation were not observed by DMSO or staphylococcal leukocidin. These data suggest that inhibition of the ADP-ribosylation by H-toxin may play an important role in potentiation of DMSO-induced differentiation of HL-60 cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenosine Diphosphate Ribose / metabolism
  • Bacterial Toxins / pharmacology*
  • Cell Differentiation / drug effects*
  • Cell Membrane / drug effects
  • Cell Membrane / metabolism
  • Clostridium
  • Dimethyl Sulfoxide / pharmacology
  • Hemolysin Proteins / pharmacology*
  • Humans
  • Tumor Cells, Cultured


  • Bacterial Toxins
  • Hemolysin Proteins
  • hemolytic toxin, Clostridium septicum
  • Adenosine Diphosphate Ribose
  • Dimethyl Sulfoxide