444 SENESCENCE AND REJUVENESCENCE 



the immortality of the protozoa, he points out that since a rapid 

 growth of protoplasm precedes each cell division, and since growing 

 protoplasm with its large volume of active breakdown is an unfavor- 

 able substratum for the accumulation of metaplasm, therefore when 

 such growth occurs the organism may frequently remain young. 

 He apparently fails entirely to note that, according to his own 

 hypothesis, elimination from the cell of metaplasmic substances 

 should make the cell more capable of active breakdown, and so 

 younger. 



Enriques ('07, '09) lays stress upon the decrease in assimilatory 

 capacity, and this capacity he believes decreases as differentiation 

 increases. Death is not a necessary consequence of life, for the 

 unicellular forms and also many plants may continue to live indefi- 

 nitely. Enriques cites some chemical analyses of plants in support 

 of his view that the nitrogenous substances become " diluted' 1 

 during development by the deposition in the cells of carbohydrates. 

 Moreover, he finds that the changes in the nitrogenous substances 

 precede the changes in other substances, and this confirms his 

 belief that the assimilatory capacity of the cells decreases, for the 

 nitrogenous substance is the assimilating substance. In other 

 words, a decrease in the proportion of chemically active protoplasm 

 occurs during development. My own views are in essential agree- 

 ment with those of Enriques, but I have endeavored to proceed 

 a few steps farther and to show how rejuvenescence occurs and its 

 significance in retarding and preventing senescence and death. 



Conklin ('12, '13) has expressed himself as in essential agreement 

 with my own conclusions concerning the nature of senescence and 

 rejuvenescence, but he lays particular emphasis upon the inter- 

 change between nucleus and cytoplasm as the fundamental condi- 

 tion of constructive metabolism, and concludes that "anything 

 which decreases the interchange between nucleus and protoplasm 

 leads to senility; anything which increases this interchange renews 

 youth.' This conclusion seems to me not sufficiently broad in 

 one sense and too broad in another. It can scarcely be doubted 

 that at least some degree of cytoplasmic or nuclear senescence may 

 occur independently of the metabolic interchange between nucleus 

 and cytoplasm, perhaps as a result of colloid or other changes in 



