Triggering Mechanisms and Inflammatory Effects of Combustion Exhaust Particles with Implication for Carcinogenesis

Basic and Clinical Pharmacology and Toxicology - Tập 121 Số S3 - Trang 55-62 - 2017
Johan Øvrevik1, Magne Refsnes1, Marit Låg1, Bendik C. Brinchmann1, Per E. Schwarze1, Jørn A. Holme1
1Department of Air Pollution and Noise Domain for Infection Control and Environmental Health Norwegian Institute of Public Health Oslo Norway

Tóm tắt

AbstractA number of biological responses may contribute to the carcinogenic effects of combustion‐derived particulate matter (CPM). Here, we focus on mechanisms that trigger CPM‐induced pro‐inflammatory responses. Inflammation has both genotoxic and non‐genotoxic implications and is considered to play a central role in development of various health outcome associated with CPM exposure, including cancer. Chronic, low‐grade inflammation may cause DNA damage through a persistent increased level of reactive oxygen species (ROS) produced and released by activated immune cells. Moreover, a number of pro‐inflammatory cytokines and chemokines display mitogenic, motogenic, morphogenic and/or angiogenic properties and may therefore contribute to tumour growth and metastasis. The key triggering events involved in activation of pro‐inflammatory responses by CPM and soluble CPM components can be categorized into (i) formation of ROS and oxidative stress, (ii) interaction with the lipid layer of cellular membranes, (iii) activation of receptors, ion channels and transporters on the cell surface and (iv) interactions with intracellular molecular targets including receptors such as the aryl hydrocarbon receptor (AhR). In particular, we will elucidate the effects of diesel exhaust particles (DEP) using human lung epithelial cells as a model system.

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Thông tin xuất bản

Basic and Clinical Pharmacology and Toxicology

Tập 121 Số S3

55-62

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