The Mechanisms of Senescence 



cribed wide variation in chromosome number. He found that 

 cells with 42 chromosomes (diploids) contribute primarily to the 

 growth of embryonic liver and to regeneration after hepatectomy 

 in adults, and that growth and restoration were apparently con- 

 fined to diploids and subdiploids. The idea of increasingly faulty 

 copying with increasing age, or of an accumulation of faulty 

 copies, is one best left for verification and assessment to the 

 cytologists, not all of whom regard the evidence for somatic 

 aneuploidy as satisfactory. Walker and Boothroyd (1953) have 

 shown that such 'aneuploidy' is easily simulated by faulty tech- 

 nique. Spurway's basic suggestion should, however, be suscept- 

 ible to verification. Clearly any evidence that the copying of 

 somatic cells deteriorates is of gerontological importance, and 

 would, if established, restore the relevance to metazoan ageing 

 of much which was formerly written concerning the senescence 

 of clones. 



6- 14 SPECIFICITY 



Campbell and Work (1953) have recently drawn attention to 

 the significance of the fact that animals cannot in general be 

 immunized against their own proteins; and they suggest that 

 the action of the genotype in determining specificity may be 

 chiefly a negative one, in the prevention rather than the 

 creation of a specific configuration. It is a matter of extreme 

 interest that the character of the proteins produced by the 

 animal body appears to change with age, as judged by calcium 

 binding power (Lansing, et at. 1949 Hansard et at. 1954, 

 serological properties (Duran-Reynals, 1940) and amino-acid 

 composition (Lansing et aL, 1951) and by the appearance of 

 collagen and elastic fibres in skin (Ejiri, 1936; Gross and 

 Schmidt, 1948, 1950). The acid-extractable collagen decreases 

 markedly with age (Banfield, 1952). In general these products 

 arise, however, not from aged cells, but from the cells of aged 

 organisms, and the change in specificity has taken place over 

 several cellular generations. It has occasionally been suggested 

 that senescence is a manifestation of an 'immune' response to 

 endogenous hormones (e.g. Picado and Rotter, 1936; Freud and 

 Uyldert, 1947). A more subtle change in specificity of cell re- 

 sponse, or of the properties of cellular products, whether it be 



169 



