SURFACE ACTION 453 



4. SURFACE ACTION 



It has been suggested immediately above that the first phase of toxi- 

 cant action is an accumulation of the active material in a peripheral 

 layer or zone outside the semi-permeable membrane. We have further 

 argued that, for most toxicants, the primary inhibitory effect is not at 

 this stage but later, after some of the toxicant has desorbed from the 

 outer zone and penetrated the protoplasm proper. However, such a 

 sharp separation of phases is only a convenience, since accumulation of 

 a foreign material is very likely to have some effects on the cell mem- 

 brane. Hypothetically we may set up three possible classes: (1) effects 

 of the sorbed toxicant are themselves lethal; (2) sorption contributes 

 to lethality by damaging the osmotic barrier and thereby facilitating 

 or making possible entrance of the toxicant into the protoplast; and 

 (3) sorption has only minor effects. 



A number of surface agents are known to be lethal to bacteria, at 

 least in part, as the result of destruction of the semi-permeable mem- 

 brane (118, 181). The antibiotic polymyxin has the same effect — 

 disruption of the osmotic barrier — in bacteria (307). The contribution 

 of lysis to lethality has, however, been questioned (398). 



Surface toxicity need not, in principle at least, be confined to effects 

 on permeability. If surface anabolic reactions are essential to growth, 

 for example, inhibition of them by a non-penetrating toxicant would 

 be sufficient. Finholt et al. (110) interpret the different toxicity of ali- 

 phatic amines in malt agar culture vis-a-vis wood block tests as indi- 

 cating that a toxicant could act externally by preventing the action of 

 an extracellular hydrolytic enzyme essential to survival. This sug- 

 gestion deserves further exploration; perhaps the most promising pos- 

 sibility is that the extracellular enzymes are actually synthesized ex- 

 teriorly to the osmotic barrier and that a toxicant might interfere with 

 the synthesis. Such an effect would be missed completely in the usual 

 assay which provides diffusible nutrients and thereby renders the fungus 

 independent of extracellular enzymes. 



The second possibility, that sorption of a toxicant might contribute 

 to lethality without being the primary event, comes to mind particu- 

 larly in relation to a few findings that toxicants at sublethal concen- 

 trations alter cell permeability. Cellular phosphorus is lost from 

 spores treated with subfungistatic doses of silver (288) or of substituted 

 s-triazines (51). Lysozyme treatment causes an increase in permeability 

 to water and, probably, to furfural (235). In bacteria, phenol increases 

 permeability to glucose; it is probable that "one-way" effects on per- 



