The Biology of Senescence 



been widely studied, though here, as in all pathological studies 

 on ageing, no line can be drawn between cause and effect. Such 

 morphological changes in pituitary cells have recently been re- 

 examined by Weiss and Lansing (1953) and by Shanklin (1953), 

 but without any new findings on the rate of cellular replace- 

 ment. In some glandular organs, such as rat salivary glands, 

 mitosis becomes both rare and abnormal in pattern after the 

 end of active body growth, while in senile rats numerous imper- 

 fect mitoses occur (Andrew, 1953). 



6-1-3 SOMATIC MUTATION 



If the copying-mechanisms of somatic cells could be shown 

 to deteriorate, like those of the Paramecium macronucleus, the 

 further they travel from the germ line, senescence might result 

 from the fact of cell turnover, not from its cessation. A possible 

 mechanism for this has been suggested to me by Dr. Helen 

 Spurway. She suggests that as a result of somatic mutation the 

 constituent cells of some mammalian tissues may lose their 

 autarky and become a 'community', in which both function 

 and the capacity for replacement have undergone distribution. 

 Such a community would contain both irreplaceable and indis- 

 pensable members, and would therefore ultimately undergo 

 senescence. 



It is clear that if mammalian tissues exhibit increasingly im- 

 perfect mitosis with increasing age, resulting in the accumula- 

 tion of aneuploid cells, this would lead to steady deterioration 

 of equilibrium. Any difference in liability to senescence between 

 mammals and lower vertebrates would be explicable, in terms 

 of this theory, on the ground that mutation rate would be higher, 

 in all probability, with higher temperatures and chromosome 

 numbers. 



This is a highly ingenious but unproven suggestion. The con- 

 tentious issue of mammalian aneuploidy generally has been 

 reviewed recently by Hsu and Pomerat (1953): a large and 

 even more contentious body of data is reviewed by Sorokina 

 (1950). Variation in chromosome number has been reported in 

 human (Andres and Jiv, 1936; Timonen and Therman, 1950; 

 Therman and Timonen 1951) and pig embryos (Sorokina, 

 1950). In adult rat liver, Tanaka (1951, 1953) recently des- 



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