نقش استرس اکسیداتیو در تکثیر بی‌رویه و مرگ سلولی

Abstract During normal cellular activities Reactive Oxygen Species (ROS) and Reactive Nitrogen Species (RNS) are produced. In addition to beneficial functions they play a critical role in cell death and prevent apoptosis. Every cell is equipped with an extensive antioxidant defense system to combat the excessive production of active radicals. Oxidative stress occurs with destruction of cellular antioxidant defense in overproduction of these reactive species induced by exogenous (e.g. ultraviolet rays) and endogenous (at the cellular level where mitochondria are involved). ROS and RNS can be beneficial or harmful to cells and tissues. At physiological low levels, reactive oxygen species act as redox messengers in intracellular signaling and regulation, whereas excess ROS induce oxidative modification of cellular macromolecules, inhibit protein function, and promote cell death. A full understanding of the redox control of apoptosis induction and inhibition can develop therapeutic interventions associated with oxidative stress-related disorders. In this review, major sources of ROS and RNS in a cell, the role of these reactive species in normal physiology and carcinogenesis and the role of antioxidants as regulators of oxidative stress and apoptosis are described. Finally, the relationship between oxidative stress and cell death are demonstrated.