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Recombinant beta-toxin from Clostridium perfringens type C was found to increase the conductance of bilayer lipid membranes (BLMs) by inducing channel activity. The channels exhibited a distribution of conductances within the range of 10 to 380 pS, with the majority of the channels falling into two categories of conductance at 110 and 60 pS. The radii of beta-toxin pores found for the conductance states of 110 and 60 pS were 12.7 and 11.1 Å, respectively. The single channels and the steady-state currents induced by beta-toxin across the BLMs exhibited ideal monovalent cation selectivity. Addition of divalent cations (Zn 2؉ , Cd 2؉, or Mg 2؉ ) at a concentration of 2 mM increased the rate of beta-toxin insertion into BLMs and the single-channel conductance, while application of 5 mM Zn 2؉ to a beta-toxin-induced steady-state current decreased the inward current by approximately 45%. The mutation of arginine 212 of beta-toxin to aspartate, previously shown to increase the 50% lethal dose of beta-toxin for mice nearly 13-fold, significantly reduced the ability of beta-toxin to form channels. These data support the hypothesis that the lethal action of beta-toxin is based on the formation of cation-selective pores in susceptible cells.

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The pitting corrosion resistance of surface-modified 316L austenitic stainless steel and N08367 (a ''superaustenitic'' stainless steel) were evaluated in 0.6 M NaCl solutions and compared to untreated samples of the same materials. The surface modification process used to treat the surfaces was a low-temperature carburization technology termed ''low-temperature colossal supersaturation'' (LTCSS). The process typically produces surface carbon concentrations of~15 at. pct without the formation of carbides. The pitting potential of the LTCSS-treated 316L stainless steel in the NaCl solution substantially increased compared to untreated 316L stainless steel, while the pitting behavior of the LTCSS-treated N08367 was unchanged compared to the untreated alloy.

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