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By Karl Maramorosch

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It has been noted (Tappel, 1968; Hochschild, 1971) t h a t membranes and proteins destroyed by lipid peroxidation are not well hydrolyzed by lysosomal enzymes, thus suggesting t h a t lipid peroxidation may be a direct cause of lysosomal engorgement. Progressive alteration and cross-linking of lipid residues in lysosomes are believed to lead to the production of lipofuscin age pigment (de Duve and Wattiaux, 1966; Tappell, 1968; Toth, 1968; Hochschild, 1971). , 26 VINCENT J. CRISTOFALO AND BETZABE M.

In contrast, Hill (1976a,b) has reported no reduction in chromatin template activity for human embryonic fibroblasts (HE 104 lines) between young (5) or middle (17) passage levels but agrees with Ryan and Cristofalo (1972) and Srivastava (1973) t h a t such decreases may occur in very late passages. In any case, if such changes do not appear until late in senescence, they cannot be considered causative (Hill, 1976a,b; Whatley and Hill, 1980a,b). Chromatin derived from confluent Phase III populations differs from t h a t derived from Phase II cells in circular dichroism spectra and in ethidium bromide binding capacity (Baserga and Nicolini, 1976).

CRISTOFALO AND BETZABE M. STANULIS-PRAEGER more readily for both the observed in vivo and in vitro behavior of dividing cell populations, but this pattern has not been generally confirmed. Perhaps the most widely known of the stochastic hypotheses is the error catastrophe hypothesis of Orgel (1963, 1970, 1973). This hypothesis suggested t h a t aging results from a random accumulation of errors occurring during replication, transcription, and translation. Originally, Orgel (1963) deduced t h a t the error frequency would increase exponentially, leading to a final "catastrophe" and death of the cell.

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