Abstract
It is suggest that when chromatin gets into a more compact state through disulfide bonding of its proteins (other kind of bonds may also play a role in the increased compactness of older chromatin), genetic activity will diminish and both transcription and replication will be more difficult and erroneous, resulting in error-containing nucleic acid and protein molecules. Involvement of translation enzyme molecules can contribute to further errors as suggested by the Orgel hypothesis (1963). Loss of important protein molecules after their genes were inactivated should also play a role in age-associated deterioration. Changes in chromatin seem to play the major part in originating age-associated deterioration of the cell. Aging should be thought of better as the result of changes of more than 1 site, and an understanding of these processes is necessary to draw a complete picture of the mechanism of aging.