抄録
One of the critical determinants of cellular response to exogenous stimuli is the cellular redox status. Intracellular generation of reactive oxygen species (ROS) is tightly regulated by the intrinsic anti-oxidant defense systems. Despite the conventional dogma that ROS are harmful to the cell, experimental evidence over the last decade that ROS also play an important role as signaling molecules in diverse physiological processes. Indeed, low levels of intracellular ROS have been linked to cellular proliferation and cell cycle progression, which provides an explanation for the pro-oxidant state invariably associated with the transformed phenotype. Contrary to that are recent observations implicating increase of intracellular ROS level in tumor cells promoting cell death signals delivered upon exposure to radiation or chemotherapeutic drugs. These studies provide convincing evidence to support a direct or indirect role for intracellular superoxide anion in creating an intracellular milieu permissive for cell death execution. Thus a novel approach to enhancing tumor cell sensitivity to radiation-induced cell death would be to favourably tailor the cytosolic milieu to allow efficient apoptotic execution. Here we present our recent data on the role of ROS in cell transformation and in the modulation of ionizing radiation-induced cell death signaling.
