108 



diet of the rat, then the animal's tail drops off (Burr and Burr). 

 It would be erroneous to conclude that the biological function of 

 these acids is to keep tails in place. 



The disturbance of any basic function must lead to disease. The 

 generation and utilization of £* is such a basic function, the dis- 

 turbance of which may declare itself in a variety of symptoms or 

 diseases. The last part of this book will be devoted to an attempt 

 to find connections between E* and "degenerative diseases." Faith- 

 ful to my traditions I will choose a degenerative disease of muscle 

 for example. The difficulties of this proposition are twofold. 

 Firstly, the physical theory of fluorescence and phosphorescence is 

 still in its infancy and so the biologist has no really firm ground to 

 stand on. This applies especially to conditions in water. Since the 

 triplets formed in water have just been found, and the water struc- 

 tures formed around nonpolar substances belong to the latest 

 achievements of science, the interaction of the two necessarily be- 

 longs to the blank spaces on our map of knowledge. Secondly, 

 even if we could understand these relations we could not state how 

 a certain change should declare itself in biological function, how, 

 for instance, the shortening or lengthening of a lifetime or a 

 change in stability of an £* should alter cell life. So in our first 

 approach we will have to content ourselves with showing that 

 changes in £* are related to changes in function, that substances 

 which affect £* also affect function and that drugs which affect 

 function affect E* . In order to prove that a drug actually could 

 have exerted its function by affecting £* we will have to show 

 that the drug is capable of affecting E* in vitro in the same con- 

 centration as it exerts its action in vivo. Unfortunately, such a nar- 

 row parallelism can be expected to exist only with drugs which 

 have no specific affinities, as was the case with 2,4-dinitrophenol. 

 Drugs with more specific structures and affinities can be expected 

 to be accumulated by their target and so exert their biological ac- 

 tion at a higher concentration than corresponds to their random 

 distribution. The higher the specificity, the greater the gap will 



