Related Experiment Video
Updated: Aug 10, 2026

Production and Detection of Reactive Oxygen Species (ROS) in Cancers
Published on: November 21, 2011
Signaling by carcinogenic metals and metal-induced reactive oxygen species
Gabriel Keith Harris1, Xianglin Shi
1National Research Council Associate, Pathology and Physiology Research Branch, National Institute for Occupational Safety and Health, 1095 Willowdale Rd. (M/S 2015), Morgantown, WV 26505-2888, USA. gharris1@cdc.gov
Abstract:
Epidemiological data indicate that exposure to metal and metalloid species, including arsenic(III), chromium(VI), and nickel(II), increases the risk of cancer, particularly of the lung and skin. Alterations in normal signal transduction as a result of exposure to carcinogenic metals, and to metal-catalyzed reactive oxygen species (ROS) formation, appear to play an important role in the etiology of metal-induced carcinogenesis. Signaling components affected by metals include growth factor receptors, G-proteins, MAP kinases, and nuclear transcription factors. This article reviews current literature on the effects of carcinogenic metals and metal-induced ROS on cancer-related signaling pathways. In addition, the mechanisms by which those changes occur, and the role of those changes in carcinogenesis are discussed.
More Related Videos
09:33Imaging Approaches to Assessments of Toxicological Oxidative Stress Using Genetically-encoded Fluorogenic Sensors
Published on: February 7, 2018
12:15Quantification of three DNA Lesions by Mass Spectrometry and Assessment of Their Levels in Tissues of Mice Exposed to Ambient Fine Particulate Matter
Published on: May 29, 2019
Related Concept Videos
Autocrine Signaling
Autocrine Signaling in Macrophages
Under normal physiological conditions, autocrine signaling is essential for maintaining homeostasis. This process is well characterized in...
Electron Transport Chain: Complex I and II
ROS generation is regulated and maintained at moderate levels necessary...
Cancer Prevention
Some...
Mutagenicity and Carcinogenicity
Bioactivation and Tissue Toxicity
Spontaneous and Induced Mutations