Effects of ageing on nuclear DNA integrity and metabolism in mussel cells (Mytilus edulis L)

As the age of a cell increases, so does the potential for DNA damage. Recen t theories on ageing suggest accumulative DNA damage is the primary cause o f cellular senescence, possibly due to the decreased ability of DNA to act as a template for gene expression. In this paper we investigate the effects of ageing on the level of nuclear DNA damage in tissues of wild mussels of three different age groups; 2-4 ye ars (group I), 6-8 years (group II) and 10 years (group III). In the digest ive land and haemolymph cells, a significant age-dependent increase of DNA damage was observed, as evaluated by the fluorimetric alkaline DNA unwindin g technique, which is able to detect both direct single strand DNA breaks a s well as alkali-labile apurinic sites. In addition, the rate of DNA polymerase activity was studied in order to de termine whether DNA damage was dependent on DNA alteration, or because of a reduced rate of DNA repair. Unscheduled DNA repair synthesis in isolated n uclei of digestive gland cells in older mussels, was significantly decrease d in comparison to younger mussels (-42% in group II and -37% in group III, p < 0.01), In the digestive gland, salt extraction gives a slight, but sig nificant, decrease of aphidicolin-sensitive DNA polymerase activity in age group III of -25%, p < 0.05, Finally, we looked at the age variation in relation to oxidative stress. Th is was evaluated by:measuring malondialdehyde accumulation in mussel cells. Digestive gland cells of group III, showed a significant age-related incre ase in malondialdehyde content of 170%, p < 0.01, indicative of enhanced pe roxidative processes. Taken together, these data suggest that the accumulation of DNA damage in g roup II is mainly dependent on the impairment of DNA repair systems. This i s contrary to group III DNA damage, where a possible relationship between o xidative stress and alteration of nuclear DNA metabolism is found, probably deriving from an antioxidant defence decline. (C) 1999 Published by Elsevi er Science Ltd. All rights reserved.