88 ENZYMES AND DRUG ACTION 



lar units, we shall not consider junctional inhibitors, but 

 only the substances acting directly upon the muscle cell 

 itself. As outstanding examples there are iodoacetate and 

 potassium. Both of these substances rapidly give rise to 

 a condition in which muscle will no longer contract. But 

 they do so by quite different mechanisms, iodoacetate 

 by preventing the synthesis of adenosine triphosphate, 

 and potassium by reducing the excitability. 



The formation of a properly functional spindle in mi- 

 tosis can be prevented by a variety of substances. These 

 include colchicine, urethan, arsenite, dithioglycerol, 

 the |S-chloroethylamines, and the sulphonamides. It 

 seems extremely improbable that substances with such 

 diverse chemical structures can be acting upon the same 

 cellular mechanism. The action of the /?-chloroethylam- 

 ines, for instance, depends upon the loss of a chloride 

 ion from the molecule with the consequent formation of 

 a carbonium ion. There appears to be no analogous pro- 

 cess possible with urethan. Then consider the two sub- 

 stances arsenite and dithioglycerol: the action of the 

 former can actually be neutralised by a moderate amount 

 of the latter. 



Lachrymation is produced as a result of the action of 

 substances upon the nerve endings in the conjunctiva. 

 Substances producing this effect include soap, osmic 

 acid and ethyl iodoacetate. It seems very improbable 

 that all these substances can be acting upon the same 

 enzyme system. 



