ROS in Carcinogenesis and Anticancerous Drug-Induced Toxicity

Equilibrium between the cell proliferation and cell death helps in maintaining cell number within a tissue and the imbalance between the two leads to cancer. Both endogenous and exogenous factors influence DNA damage, cell growth, and cell death and contribute to carcinogenesis. There are experimental evidences to support the role of reactive oxygen species in the cancer process. Increase in reactive oxygen species in the cell, through either biological modification or chemical exposure to carcinogen, contributes to the process of carcinogenesis. As already stated, reactive oxygen species can arise through a variety of factors and pathways. Oxidative stress due to these can directly lead to production of single- or double-stranded DNA breaks, purine, pyrimidine, or deoxyribose modifications, and DNA cross-links. Persistent DNA damage can result in either arrest or induction of transcription, induction of signal transduction pathways, replication errors, and genomic instability, all of which are seen in carcinogenesis. Oxidative stress also plays a dual role in inducing toxicity due to administration of drugs given to treat cancer aggregation which further lead to toxicity in various organs and tissues such as cardiotoxicity, neurotoxicity.