Abstract
DNA-repair capacity, by incorporation in vitro of [ 3H]thymidine into DNA of isolated neuronal cells and spleenic lymphocytes of rat was studied as a function of age. The incubations were carried out both in presence and absence of hydroxyurea (HU), a known inhibitor of replicative DNA synthesis. The results indicate that neurons, unlike lymphocytes, obtained from adult and old animals offer a good model system to measure the DNA-repair process without any possible interference of DNA replicative synthesis. Further, the ‘spontaneous’ DNA repair by unscheduled DNA synthesis (UDS) in old neurons remained unchanged as compared to the adult level. However, the response of aging neurons, in contrast to that of young and adult neurons or of lymphocytes of any age, to a mutagenic challenge like UV lights is limited. It is suggested that this lack of responsive DNA-repair against a given damage may lead to a general metabolic deterioration and senescence.
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