Growth and Senescence 



chemical states and gradients. That adjacent-cell effects need 

 not depend upon molecular hormones is well shown by Whita- 

 ker's work on the mutual orientation of Fucus egg cells through 

 a simple pH gradient (see J. Needham, 1942). The search for 

 hormonal substances which can be isolated is abundantly justi- 

 fiable, but the failure to find them should not be astonishing or 

 discouraging. There is much evidence (reviewed by Stewart 

 and Kirk, 1954) to suggest that the 'inhibitors' detected in old 

 serum by Carrel and his associates were nonspecific materials, 

 probably including the serum lipoproteins. This is not to say 

 that such materials do not exert a growth-inhibiting effect in 

 vivo, or that such an effect is without physiological significance, 

 but most existing studies certainly support Medawar's conclu- 

 sion (1942) that there is no simply extractable contact hormone 

 in adult tissue which directly restrains the growth of cells. The 

 'inflection 5 in the curve of absolute growth (weight/time) is still 

 occasionally quoted as evidence of active growth-inhibition, but 

 this is a mathematical fallacy which has been repeatedly ex- 

 posed (Minot, 1908; Schmalhausen, 1929; Weymouth, 1931; 

 Medawar, 1945). 



The most interesting aspect of this question, in relation to 

 senescence rather than morphogenesis, turns once again on the 

 supposed absence of age changes in some reptiles and fish, 

 though speculation is vain so long as we do not know whether 

 this absence is real. The growth of the body, and of the indi- 

 vidual organs, in some of these forms follows much the same 

 pattern of decline as that described by Medawar in the growth 

 energy of isolated tissues. If reptiles whose growth declines in 

 this way, and whose degree of histological complexity is in any 

 case similar to that found in mammals, do not exhibit sen- 

 escence, then this general pattern of growth-decline with age, 

 although it occurs in many mammalian tissues treated indi- 

 vidually, is not the 'cause' of mammalian senescence. Equili- 

 brium cessation of growth implies the probability of one-for-one 

 replacement in tissues which are capable of continuing division, 

 so that unless some other process intervenes, an organism in the 

 equilibrium state as regards growth should remain indefinitely 

 self-maintaining, except for tissues whose degree of differen- 

 tiation precludes mitotic renewal. This seems a reasonable 



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