The Level of ROS and DNA Damage Mediate with the Type of Cell Death, Senescence or Apoptosis

Cell senescence, originally defined as the proliferative arrest that occurs in normal cells after a limited number of cell divisions, is now more broadly regarded as a general biological program of terminal growth arrest. Replicative senescence of cells due to telomeric changes exhibits similar features with those seen in DNA damage (Vaziri et al., 1997; von Zglinicki, 2001). Therefore, DNA damage is expected to induce rapid cell growth arrest, which would be phenotypically indistinguishable from replicative senescence (Di Leonardo et al., 1994). This type of accelerated senescence that does not involve telomere shortening is triggered in normal cells by the expression of supraphysiological mitogenic signals (Orr et al., 1994). Not only normal cells, but also cancer cells can be induced readily to undergo senescence by genetic manipulation or by treatment with chemotherapeutic agents, radiation, or differentiating agents.