ANTITOXINS II 



hitherto exerted by the cells destroyed by the 

 irritant; and, finally, when such bioplastic activity 

 is called into play there is always hypercompen- 

 sation i.e. there is more plastic material gene- 

 rated than is necessary to compensate for the 

 loss. 



Ehrlich points out that owing to the combination 

 of the toxin with the side chain of a cell, these 

 side chains are practically lost to the cell ; that the 

 latter or its fellows now produces new side chains to 

 replace this loss, but that this production always 

 goes so far as to make a surplus of side chains ; that 

 these side chains are thrown off by the cell as 

 unnecessary ballast, and then circulate in the blood 

 as antitoxin. The same substances, therefore, which 

 when part of the cell combine with the haptophore 

 group of the toxin, enabling that to act on the cell, 

 when circulating free in the blood combine with 

 and satisfy this haptophore group of the toxin, 

 and prevent the poison from combining with and 

 damaging the cells of the organism. 



It does not follow from Ehrlich's theory that the 

 antitoxin is produced by the same set of cells whose 

 injury by the toxin gives rise to the particular 

 clinical symptoms. Thus we might believe that 

 although in tetanus the cells of the central nervous 

 s}^stem give rise to the characteristic symptoms, cells 

 entirely apart from these, e.g., in the bone marrow, 

 might be the main source of the antitoxin. The 



