Abstract
Tobacco smoke and radioactive radon gas impose a high risk for lung cancer. The radon-derived ionizing radiation and some components of cigarette smoke induce oxidative stress by generating reactive oxygen species (ROS). Respiratory lung cells are subject to the ROS that causes DNA breaks, which subsequently bring about DNA mutagenesis and are intimately linked with carcinogenesis. The damaged cells by oxidative stress are often destroyed through the active apoptotic pathway. However, the ROS also perform critical signaling functions in stress responses, cell survival, and cell proliferation. Some molecules enhance radiation-induced tumor cell killing via the reduction in DNA repair levels. Hence the DNA repair levels may be a novel therapeutic modality in overcoming drug resistance in lung cancer. Either survival or apoptosis, which is determined by the balance between DNA damage and DNA repair levels, may lender the major problems in cancer therapy. The purpose of this paper is to take a closer look at risk factor and at therapy modulation factor in lung cancer relevant to the ROS.
Highlights
Lung cancer is the commonest fatal cancer whose risk is dependent on the number of cigarettes smoked per day as well as the duration years of the smoking [1, 2]
A wide variety of the other toxic substances such as asbestos, polycyclic aromatic carbohydrates, arsenic, and diesel emissions have been identified as potential causes of lung cancer [4, 5]. Some of these carcinogens react covalently with DNA to cause oxidative damage, which can induce DNA breaks [6]. Another recognized lung carcinogen is the chemically nearly inert gas radon [7], a ubiquitous natural air pollutant arising from radioactive decay of the uranium-238, which is present throughout the earth crust
reactive oxygen species (ROS) appear to play an essential role as secondary messengers in the normal regulation of a variety of physiological processes, such as apoptosis, survival, and proliferative signaling pathways [9, 10]
Summary
Lung cancer is the commonest fatal cancer whose risk is dependent on the number of cigarettes smoked per day as well as the duration years of the smoking [1, 2]. A wide variety of the other toxic substances such as asbestos, polycyclic aromatic carbohydrates, arsenic, and diesel emissions have been identified as potential causes of lung cancer [4, 5] Some of these carcinogens react covalently with DNA to cause oxidative damage, which can induce DNA breaks [6]. Another recognized lung carcinogen is the chemically nearly inert gas radon [7], a ubiquitous natural air pollutant arising from radioactive decay of the uranium-238, which is present throughout the earth crust. As ROS are produced in all mammalian cells from mitochondrial oxidative respiration, cellular defense mechanisms have evolved to protect cells from ROS [11] Those include DNA repair systems and detoxifying scavenger enzymes such as superoxide dismutases [12]. We summarize the function of DNA repair molecules at a viewpoint of carcinogenic DNA damage and cancer therapy modulation involved in lung cancer
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
