Abstract
Reactive oxygen or nitrogen species (ROS, RNS) and oxidative stress in the respiratory system increase the production of mediators of pulmonary inflammation and initiate or promote mechanisms of carcinogenesis. The lungs are exposed daily to oxidants generated either endogenously or exogenously (air pollutants, cigarette smoke, etc.). Cells in aerobic organisms are protected against oxidative damage by enzymatic and non-enzymatic antioxidant systems. Recent epidemiologic investigations have shown associations between increased incidence of respiratory diseases and lung cancer from exposure to low levels of various forms of respirable fibers and particulate matter (PM), at occupational or urban air polluting environments. Lung cancer increases substantially for tobacco smokers due to the synergistic effects in the generation of ROS, leading to oxidative stress and inflammation with high DNA damage potential. Physical and chemical characteristics of particles (size, transition metal content, speciation, stable free radicals, etc.) play an important role in oxidative stress. In turn, oxidative stress initiates the synthesis of mediators of pulmonary inflammation in lung epithelial cells and initiation of carcinogenic mechanisms. Inhalable quartz, metal powders, mineral asbestos fibers, ozone, soot from gasoline and diesel engines, tobacco smoke and PM from ambient air pollution (PM10 and PM2.5) are involved in various oxidative stress mechanisms. Pulmonary cancer initiation and promotion has been linked to a series of biochemical pathways of oxidative stress, DNA oxidative damage, macrophage stimulation, telomere shortening, modulation of gene expression and activation of transcription factors with important role in carcinogenesis. In this review we are presenting the role of ROS and oxidative stress in the production of mediators of pulmonary inflammation and mechanisms of carcinogenesis.
Highlights
Studies of pulmonary carcinogenicity and respiratory inflammation have shown high risk for respiratory diseases and lung carcinogenesis in humans from exposures to various inhalable dusts, mineral fibers, airborne particulate matter (PM) and ozone
Studies showed that modulation of gene expression by reactive oxygen species (ROS) and reactive nitrogen species (RNS) and the resulting oxidative stress is an important mechanism of carcinogenesis
In this review we presented the most important and recent studies concerning the role of ROS, RNS
Summary
Studies of pulmonary carcinogenicity and respiratory inflammation have shown high risk for respiratory diseases and lung carcinogenesis in humans from exposures to various inhalable dusts, mineral fibers, airborne particulate matter (PM) and ozone. Tobacco smoke plays a very important role in increasing the risk for epithelial inflammation and lung cancer due to its high carcinogenic potential and the synergistic effects with other respirable particulate to generate reactive oxygen species (ROS) and catalyze redox reactions in human lung epithelial cells, leading to oxidative stress and increased production of mediators of pulmonary inflammation [5,6,7,8,9]. Free radicals and ROS are hazardous for living organisms and can cause oxidative damage to all major cellular constituents (membrane lipids, proteins, enzymes, DNA).
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