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By Karl Maramorosch

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Extra info for Advances in cell culture. Volume 2

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This suggests t h a t the altered template activity is an effect rather t h a n a cause of aging. , 1980). Bowman et al. (1976a) have reported t h a t the age-related decline in RNA synthesis in WI-38 cells is due entirely to decreased synthesis of nucleolar RNA. However, in resting, nongrowing embryonic lung fibroblast lines, including the WI-38 line, the amount of rRNA and mRNA were both reduced nearly 2-fold in comparison to growing cultures while polysome-associated RNA was reduced about 4-fold (Meedel and Levine, 1977).

In any case, a number of phenotypic differences including an indefinite life span characterize h u m a n cells transformed by SV40 (Sack, 1981). Unfortunately, the mechanism by which "immortality" is achieved is still obscure. At first glance it would appear t h a t transformation is unlikely to shed light on the mechanisms of senescence since the transformed cells have acquired abnormal characteristics. On the other hand, SV40 transformation probably represents a potentially powerful probe for understanding the mechanisms regulating senescence.

Ove and Coetzee (1978) have found t h a t bleomycin, a stimulator of DNA repair, caused a 2-fold higher incorporation of tritiated thymidine triphosphate in liver cell nuclei from middle-age rats as compared to old suggesting diminished repair capacity in old rats. Likewise, Epstein et al. (1973,1974) have reported that normal human skin fibroblasts show decreased repair of 7-ray-induced DNA chain breaks with increasing in vitro age. A similar finding of decreased repair in progeria cells by this group has not been confirmed (Regan and Setlow, 1974).

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