146 K. BAHADUR 



ation of 2450-2500 A, i.e., of shorter wavelength than the primary- and even of 

 stronger intensity than the primary radiation is emitted [29]. And Wolff & Ras [30] 

 observed a similar effect with sterile blood serum, which produced secondary 

 radiations similar to the above when bacteria have grown in it. 



It has been observed by Gurwitsch [31] and Korosi [32] that certain molecules 

 which are capable of enzymic cleavage can react on mitogenetic radiations and 

 themselves become radiant. Differently charged centres of these molecules are 

 activated differently by the irradiating Ught to emit mitogenetic radiations. 



Latmanisowa [35], studying the secondary radiations from nerves after mito- 

 genetic radiations, observed that the induction effect of secondary rays is very 

 strong in the begiiming, starts decreasing after five minutes and disappears after 

 thirty minutes and does not appear any more on continuous exposure. Gurwitsch 

 [37] observed similar loss in the power of secondary radiations of radiating cells 

 or tissues when they themselves are exposed to mitogenetic rays. Even good 

 radiating cultures lose their power of radiation when exposed to their own 

 wavelength. Overdose of radiation causes retardation in the emission of secondary 

 radiations. Gurwitsch called this phenomenon mitogenetic depression [33], 

 Salkind observed a retardation in the secondary emission of rat blood [34]. 

 Correlating these data we can safely conclude that the macromolecular aggregate, 

 when exposed to certain radiations, will emit secondary radiations of different 

 wavelength and magnitudes depending upon the nature of bonds which are 

 decomposed or synthesized, upon the atoms taking part in the reactions, and 

 upon the wavelength and magnitude of the initiating radiations. 



It is found that the mitogenetic radiations emitted by protein molecules on 

 irradiation cease after a certain period of irradiation [33-35]. This is due to 

 the fact that the protein molecule has a more or less fixed structure and the 

 irradiation can introduce only a Hmited possibility of further permutations and 

 combinations, under the influence of the free radicals thus formed. On the other 

 hand the macromolecular aggregate has infinite possibilities of permutation and 

 combination within the same molecule and so can continue emitting mitogenetic 

 radiations for a long time till a stable structure is achieved. The macromolecule 

 can also combine with other molecules synthesized photochemically, giving rise 

 to further emission of mitogenetic radiations. The resulting compound if un- 

 stable will also emit radiations, because in its attempt to attain a stable state it 

 will of a necessity disturb the fluctuating electrostatic forces of the molecular 

 system. A similar type of mitogenetic radiation is observed when an enzyme 

 reacts on a substrate [31, 32]. 



When a mixture of paraformaldehyde and potassium nitrate in water is ex- 

 posed to light in the presence of a suitable catalyst, a dynamic mbcture of amino 

 acids is formed. These amino acids are constantiy changing from one to another 

 and these combine with one another to form macromolecular aggregates. And 

 thus the whole mixture forms a continuous source of mitogenetic radiations for 

 a long time when irradiated. 



In these molecular changes, only those changes, which involve the formation 

 of molecules at the same thermodynamic energy level or at littie energy-level 

 difference, help in keeping up a continuous emission. If the molecular changes 



