Oxidative Stress and Inflammatory Factors in Lung Cancer

Abstract

Abstract Reactive oxygen species (ROS) are involved in both cancer generation and therapy. Lung carcinogenesis agents, such as tobacco-smoking or inorganic substances, exert their carcinogenic effects through oxidative stress. The presence of a chronic inflammatory microenvironment, which is associated with oxidative stress, is also important in carcinogenesis. Conversely, some antineoplastic agents, including radiation and chemotherapeutics, exert their antineoplastic effect by inducing cell damage via ROS-mediated toxicity. Since the production of ROS can also cause cell injury, by stimulating lipid peroxidation, increasing the substrate for lipid peroxidation in tumor cells may be an important goal in improving the effects of antineoplastic agents. Some studies suggest that n-3 polyunsaturated fatty acids (PUFAs) enhance oxidative stress in cancer cells and, at the same time, decrease the inflammatory response during radiotherapy and chemotherapy; they might thus be considered a preliminary goal in anticancer and anticachectic therapy.