The Mechanisms of Senescence 



of the adult animal is virtually confined to such tissues as skin, 

 and that the 'cause' of senescence resides in the exhaustion 

 of endocrine cells which have accompanied the individual 

 throughout life. This may be true of some invertebrates, many 

 of which have a wholly determinate cell-number throughout, 

 or in certain organs, such as the corpus allatum of bees (Pflug- 

 felder, 1948) and the suggestion cannot be refuted in terms of 

 individual cells in man and other mammals. Such irreplace- 

 ables may exist, but the idea is in many ways open to the same 

 criticism as that which attributes ageing to changes in bio- 

 logically inert colloids, and the body of evidence suggests that 

 it is equally erroneous. Although the rate of turnover in liver 

 cells decreases with age, and mitotic figures become few, the 

 mean mitosis rate in adult rats is such as to double the volume 

 of the organ in the animal's lifetime, if there were no incidental 

 wastage. 1 This figure suggests that some liver cells may accom- 

 pany the animals from cradle to grave, but that the majority 

 do not. Adrenal cortical cells are continuously replaced in the 

 adult cat (Lobban, 1952). Mitotic activity does, however, 

 appear to decrease with advancing age (Blumenthal, 1945; 

 Townsend, 1946; Korenchevsky, Paris and Benjamin, 1950). 

 The adrenals of old rats show various degenerative changes 

 (Jayne, 1953). Mitosis varying in frequency with the sexual 

 cycle occurs in the anterior pituitary (Hunt, 1942, 1943, 1947) 

 though it may not affect all cell types equally, since the popula- 

 tion changes in composition with advancing age (Parsons, 1936) . 

 There is no direct evidence that the power of cell replacement 

 is lost in any endocrine gland with age, though there may be 

 more general involutional changes at both cellular and tissue 

 levels. The pattern of mammalian endocrine cell behaviour is 

 predominantly one of continual division and replacement, 

 regulated in level by hormonal influences, and often occurring 

 in cycles. It is impossible to say at present whether there is a 

 single key exception to this pattern, but ageing is unlikely to be 

 so simple a matter as the defection of one type of cell. It is 

 significant that the syndrome of senescence cannot be produced 

 experimentally by extirpating any one gland. 



The morphological changes in endocrine cells with age have 

 1 I am indebted to Mr. M. Abercrombie for this figure. 



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