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Oxidative Stress and Pulmonary Carcinogenesis Through Mechanisms of Reactive Oxygen Species. How Respirable Particulate Matter, Fibrous Dusts, and Ozone Cause Pulmonary Inflammation and Initiate Lung Carcinogenesis

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Oxidative Stress in Lung Diseases

Abstract

The majority of new cases of cancer worldwide in 2012 were lung cancers (1.8 million). Epidemiologic studies established that the most important risk factor for lung cancer is tobacco smoking (active and passive). Other factors which contribute substantially are occupational exposures to carcinogenic chemicals; vehicular air pollution in urban and industrial areas; environmental exposure to inorganic dusts and asbestos fibers; certain carcinogenic metals Cd, As, and Cr; and indoor air pollution. Lungs are exposed to air oxidants generated either endogenously or exogenously, but aerobic organisms are protected against oxidative damage by enzymatic and low molecular weight nonenzymatic antioxidants. Lung cancer mechanisms are promoted through the generation of reactive oxygen and nitrogen species (ROS/RNS) as a result of oxidative stress and exposure to external air pollutants, leading to oxidative stress and inflammation. Their role in the initiation and progression of cellular and mitochondrial DNA damage (cDNA and mtDNA), membrane lipid peroxidation, and oxidative damage to proteins and enzymes is crucial. Also, airborne particulate matter (PM10 and PM2.5) are microparticles or nanoparticles which can penetrate the respiratory system, entering deep into the lung alveoli and trapped in the interior. Physical and chemical characteristics of particles (size, transition metal content, speciation, stable free radicals, etc.) play an important role in oxidative stress. Chronic exposures to these air pollutants initiate the synthesis of mediators of pulmonary inflammation in lung epithelial cells and promote the initiation of carcinogenic mechanisms. Inhalable quartz, metal powders, mineral asbestos fibers, ozone, soot from gasoline and diesel exhausts, tobacco smoke, and PM10 and PM2.5 are involved in various oxidative stress mechanisms. Pulmonary cancer initiation and promotion have 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. This review presents the role of ROS and oxidative stress in the production of mediators of pulmonary inflammation and the promotion of mechanisms of carcinogenesis.

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Authors and Affiliations

  1. Department of Chemistry, National and Kapodistrian University of Athens, Athens, Greece

    Athanasios Valavanidis

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  1. Athanasios Valavanidis
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Correspondence to Athanasios Valavanidis .

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Editors and Affiliations

  1. Department of Biochemistry and Biophysics, University of Kalyani, Kalyani, West Bengal, India

    Sajal Chakraborti

  2. Department of Biochemistry and Biophysics, University of Kalyani, Kalyani, West Bengal, India

    Tapati Chakraborti

  3. Department of Biochemistry and Cancer Biology, Meharry Medical College, Nashville, TN, USA

    Salil Kumar Das

  4. Amity University, Kolkata, West Bengal, India

    Dhrubajyoti Chattopadhyay

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Valavanidis, A. (2019). Oxidative Stress and Pulmonary Carcinogenesis Through Mechanisms of Reactive Oxygen Species. How Respirable Particulate Matter, Fibrous Dusts, and Ozone Cause Pulmonary Inflammation and Initiate Lung Carcinogenesis. In: Chakraborti, S., Chakraborti, T., Das, S., Chattopadhyay, D. (eds) Oxidative Stress in Lung Diseases. Springer, Singapore. https://doi.org/10.1007/978-981-13-8413-4_13

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