By Karl Maramorosch
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Extra info for Advances in cell culture. Volume 2
An inverse correlation had been previously found between species life span and the ability of cultured fibroblasts to activate DMBA to mutagenic form (Schwartz, 1975). , 1980) in studies of a large number of species have found that the relationship between species life span and DNA repair is not well defined. As a whole, these results suggest t h a t there may be a relationship between DNA repair capacity and cellular aging, but they do not support the concept t h a t decline in the efficiency or fidelity of DNA repair is causal or contributory to aging (Little, 1976).
On the other hand, nearly 100% of chick cells enter DNA synthesis throughout the entire life span of the culture (Lima and Marcieira-Coelho, 1972). Senescing mouse embryo cells, after showing a progressive decline in the percentage of cells able to incorporate [ 3 H]thymidine, are overgrown by a population of cells that actively incorporates [ 3 H]thymidine (Meek et aL, 1977). Subsequently, cells from the second population form tumor cells when tested in vivo. A slight decrease in cellular DNA content has been observed in senescent h u m a n diploid cells in both the Gx and G 2 + M phases (Schneider and Fowlkes, 1976).
Stein (1976) has found t h a t two DNA-binding proteins are present in above normal amounts in SV40-transformed WI-38 cells, in HeLa cells, and in chemically transformed human liver cells. Two tumor cell lines lacking one of these proteins was sensitive to density-dependent inhibition of replication. The relationship of DNA-binding proteins to cellular aging has been well delineated by Stein (1975) who has isolated such proteins from young and old WI-38 cells in both the replicative and stationary phases of growth.