Growth and Senescence 



acquisition by certain zooids of inhibitory powers over the 

 development of others (Summers, 1938), although the inhibited 

 cells retain the potentiality of growth. It is also known that 

 some 'old 5 tissue cells are capable of indefinite growth in 

 cultivation. 



The suggestions implicit in this type of reasoning are tempt- 

 ing, but there are evidential grounds for caution in postulating 

 a simple, 'toxic' senescence due to the existence of a growth- 

 inhibiting senile principle. Such a principle is not readily 

 demonstrated. Bidder once rashly located it in the pineal gland. 

 Kotsovsky (1931) attempted successfully to retard the growth 

 of tadpoles by feeding senile heart muscle — an improbable 

 tissue for such a purpose — and Grimm (1949) obtained similar 

 results with senile plasma. Picado (1930) enhanced the growth 

 of young rats by transfusions of adult plasma. More serious data, 

 however, exist. 



The best experimental evidence concerning growth-limitation 

 is probably that obtained from studies of mammalian liver. 

 Although mitotic figures and binucleate cells decrease in mam- 

 malian liver throughout life, regeneration after hepatectomy 

 occurs in senile rats, apparently at a rate not much lower, so 

 far as replacement of cell number of concerned, than in young 

 adults, though much less than in growing animals (Bucher and 

 Glinos, 1950). As Minot pointed out (1908) the adult differs 

 more from the infant than the old from the adult. The time lag 

 between hepatectomy and maximum mitotic count increases 

 with age (Marshak and Byron, 1945), thereby paralleling the 

 difference between the behaviour of tissues from young imma- 

 ture and young adult donors in tissue culture (Hoffman, Gold- 

 schmidt and Doljanski, 1937), and confirming the universal 

 finding of increased growth-inertia, rather than decreased 

 growth capacity, as the most conspicuous character of cellular 

 explants with increasing donor age (Gohn and Murray, 1925; 

 Suzuki, 1926; Medawar, 1940). In regenerating rat liver at all 

 ages, however, the lag reverts to the value characteristic of 

 young animals (Glinos and Bartlett, 1951). In young, actively 

 growing rats the restoration of liver mass after hepatectomy 

 shows a considerable rebound phenomenon, reaching 145 per 

 cent of the original weight in 7 days (Norris, Blanchard and 



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