Abstract

It is well known that oxidative stress can lead to chronic inflammation which, in turn, could mediate most chronic diseases including cancer. Oxidants have been implicated in the activity of crocidolite and amosite, the most powerful types of asbestos associated to the occurrence of mesothelioma. Currently rates of mesothelioma are rising and estimates indicate that the incidence of mesothelioma will peak within the next 10-15 years in the western world, while in Japan the peak is predicted not to occur until 40 years from now. Although the use of asbestos has been banned in many countries around the world, production of and the potentially hazardous exposure to asbestos is still present with locally high incidences of mesothelioma. Today a new man-made material, carbon nanotubes, has arisen as a concern; carbon nanotubes may display 'asbestos-like' pathogenicity with mesothelioma induction potential. Carbon nanotubes resulted in the greatest reactive oxygen species generation. How oxidative stress activates inflammatory pathways leading to the transformation of a normal cell to a tumor cell, to tumor cell survival, proliferation, invasion, angiogenesis, chemoresistance, and radioresistance, is the aim of this review.

Highlights

  • Oxidative stress is defined as an imbalance between the production of free radicals and reactive metabolites, socalled oxidants or reactive oxygen species (ROS), and the ability of a biological system, named antioxidant, to readily detoxify reactive intermediates or repair the resulting damage [1]

  • Free radicals generated from asbestos fibers and/or damages by fibers can alter biological macromolecules including proteins, cell membrane lipids, deoxyribonucleic acid (DNA), and ribonucleic acid (RNA) resulting in the initiation of numerous signal transduction pathways that are linked to inflammation, malignant transformation, proliferation, and apoptosis

  • Mesothelial cells internalize the fibers via integrins or other receptors; fibre uptake was found in some studies to be necessary for adverse effects of the fibers such as ROS generation, DNA damage, and apoptosis [30]

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Summary

Introduction

Oxidative stress is defined as an imbalance between the production of free radicals and reactive metabolites, socalled oxidants or reactive oxygen species (ROS), and the ability of a biological system, named antioxidant, to readily detoxify reactive intermediates or repair the resulting damage [1]. Chronic inflammation triggered by asbestos exposure leads to increased production of ROS from inflammatory cells, or alteration of immunocompetent cells and later reduction of tumor immunity [24, 25]. Free radicals generated from asbestos fibers and/or damages by fibers can alter biological macromolecules including proteins, cell membrane lipids, deoxyribonucleic acid (DNA), and ribonucleic acid (RNA) resulting in the initiation of numerous signal transduction pathways that are linked to inflammation, malignant transformation, proliferation, and apoptosis.

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