Role Of Oxidative And Nitrosative Stress In Carcinogenesis

Oxidative and nitrosative stress occurs when the rate of production of ROS and RNS exceeds the antioxidant capability of the cell. In such cases, ROS/RNS interact with and modify the cellular proteins, lipids, and DNA, which results in altered target cell function. Excess ROS results in either alterations of DNA structure, such as point mutations or sister chromatid exchange, and chromosomal aberrations.6'19'26 ROS and RNS cause alkylation, hydroxylation, and nitration of DNA bases. Unrepaired DNA damage results in the formation of new mutations and potentially new initiated cells that are promoted to neoplastic growth.27 Mutations in nucleic acids also prevent binding of proteins at specific DNA sites, thus affecting transcription factor binding and signaling pathways and altering expression patterns of stress response genes. ROS- and RNS-initiated pathways of signal transduction, such as mitogen-activated protein kinases (MAPK) or the transcription factors, nuclear factor kappaB (NF-kB) and activator protein-1 (AP-1), eventually determine the course of cellular apoptosis and

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