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The loss of cellular function during the ageing process is a consequence of the cumulative damage caused by reactive oxygen species produced during normal aerobic metabolism [l]. The deleterious effects of free radical damage may be counterbalanced by the cell’s antioxidant defence mechanism [2], an extremely complex system consisting of detoxifying enymes, low molecular weight antioxidant molecules and repair and turnover processes. When the free radical load increases over and above the capacity of the antioxidant system or the antioxidant system becomes less effective, then the cell is in a state of “oxidative stress’ 131. According to the free radical theory, ageing is the result of chronic oxidative stress [l].

Oxidative stress in cell culture can be generated in many different ways. The cell’s antioxidant defences can be compromised by, for example, inhibiting catalas0 activity by 3-aminotriazole or depleting glutathione levels using buthionine sulphoximine. The levels of exposure to reactive oxygen species may beartificially elevated by employing y-radiation, elevating oxygen tension (hyperoxia)[4] by extracellular 0%[5] and HzOz [6] or free radical generators. In this communication human hepatoma cells (HepG2) were challenged with the well-known water-soluble radical initiator 2, 2’-azobis (2-