ISSN 2630-0583 (Print)
ISSN 2630-0656 (Online)
Journal of Current Science and Technology
Rangsit Journal of Arts and Sciences. Vol.4 No.2 , July - December 2014.
Roles of reactive oxygen species (ROS) in inflammation and cancer
Cancer can be caused by either endogenous (genetic disorders and impairments of the immune system) or exogenous (environmental, carcinogen, infection, and persistent inflammation) factors. Inflammation is an important physiological defense response of the biological system to protect cells or tissues from injury or infection. Acute inflammation occurs over a short duration as part of the normal defense response, while chronic inflammation is a prolonged reaction related to various diseases including carcinogenesis. Many types of immune cells are involved directly or indirectly in chronic inflammation in the production of inflammatory cytokines and it appears that chronic inflammation predisposes susceptible cells to mutation (s). Reactive oxygen species (ROS) are one of the mediators produced by inflammatory cells to eradicate invading pathogens. Persistent production of ROS during chronic inflammation can overcome antioxidant defenses leading to intense oxidative stress. Consequently, cellular structures and DNA become damaged, which is a critical aspect of carcinogenesis. Notwithstanding, ROS can induce apoptotic cell death when cells are exposed at optimum levels and time to ROS. ROS generation through radiotherapy and some types of chemotherapy is therefore a goal of cancer treatment. Care must be taken, however, as ROS can cause serious side-effects. This paradoxical effect of ROS—carcinogenesis vs. cancer therapy—depends on the level intracellular ROS and exposure time. In this review, we reported the associations of chronic inflammation, ROS and carcinogenesis as well as the role of ROS in cancer treatment. The mechanism of the association of ROS with inflammation and carcinogenesis remain inconclusive, so several research studies have focused upon investigating these phenomena.