The complexity of responses to DNA damage, which involve networks of interacting processes, including DNA repair mechanisms, cell cycle checkpoints and apoptotic pathways, means that the cellular processes of DNA damage responses and DNA repair and how these impact on organismal processes like ageing are only partly understood.Elucidating the evolution of these mechanisms and how adaptations in them could have contributed to species differences in ageing also remains a promising but daunting task.Advances in data integration, modelling and highthroughput approaches have the potential to elucidate the complex interplay between DNA damage, DNA repair, and their interacting networks, but there is still a long road ahead.Ultimately, however, such approaches can lead to solving ageing, one of the greatest biological riddles of our time.We apologize to those whose work could not be cited due to lack of space.Comp. Physiol. B. This cell line effectively repairs DNA damage induced by irradiation.DNA damage induced by neutrophils was correlated with the oxidative burst of the neutrophils.The levels of superoxide anion, HO, and HOC produced after stimulation of the neutrophils were. pM respectively in min.The results of alkaline elution experiments revealed that when the same concentration of neutrophils was coincubated for min in serumfree medium with an equal number of radioactively labeled RIMPC cells, the latter incurred a level of damage that approximated that caused by rad equivalents of irradiation or by a min treatment with tM H at C.Damage from neutrophils was coincident with the oxidative burst; it was induced rapidly but remained high for more than min.Finally, repair of strand breaks induced by neutrophils was significantly slower than that observed for repair of similar levels of damage induced by HO or irradiation. The results indicate that neutrophils cause prolonged DNA damage in neighboring cells.Moreover, they indicate that although HO produced in the oxidative burst is an essential mediator of the damage observed, additional reactive oxygen intermediates including the superoxide anion are also implicated.Although the mechanism whereby inflammation may initiate or promote tumorigenesis is not known, it is hypothesized that inflammatory phagocytes may mediate this process by inflicting damage to the DNA of susceptible neighboring cells residing at the site of inflammation and activated macrophages by inflammatory compounds and tumor promoters results in activation of a respiratory burst in which a variety of reactive oxygen intermediates. These include the superoxide anion, HO, and numerous secondary labile and long lived oxidants. We have been interested in elucidating the possible role of inflammatory phagocytes in promoting murine plasma cell tumorigenesis.Plasmacytomas develop histologicalry in the oil granuloma.Over of pristaneinduced plasmacytomas have characteristic chromosomal rearrangements that involve breaks within or near cmyc on chromosome is not known and mouse plasmacytoma induction provides a model to investigate their origin.As pristane itself is not thought to be genotoxic, secondary mutagenic factors must be sought.Establishment of first generation transplant cells in culture and cell cloning were carried out as described previously containing RPMI. mercaptoethanol, tgml transferrin, igml low density lipoproteins. Splenic perfusates that were freed of erythrocytes by hypotonic lysis in NR, C.