Metals such as lead (Pb), nickel (Ni), and chromium (Cr) are pervasive and persistent environmental contaminants employed in a number of industrial processes and articles that are used by millions of people. Compelling evidence indicates that chronic exposure to these chemicals is associated with serious human pathologies including inflammatory disorders and cancer. However, the precise mechanisms underlying metal-induced toxicity and carcinogenicity are not completely understood and in most of the cases appear to be largely dose-dependent and context-dependent. It is becoming increasingly clear that Pb, Ni, and Cr species have the ability to alter the intracellular redox homeostasis and promote oxidative stress through the increased accumulation of ROS and the inactivation of key antioxidant systems. As a consequence, highly reactive free radicals can induce oxidative modifications to the macromolecules including DNA, lipids, and proteins that initiate carcinogenesis at the earlier stages while creating a microenvironment favorable to tumor progression at later stages. In light of the recent advances, the induction of oxidative stress and the overproduction of intracellular ROS appears to be a common mechanism of metal-induced carcinogenesis that has received great attention in the field of cancer research. This chapter briefly reviews the role of ROS production in chemical carcinogenesis induced by Pb, nickel Ni, and Cr, metals with the ability to induce cancer development in either humans or animals and to promote ROS accumulation as observed in many studies.
|Title of host publication||Handbook of Oxidative Stress in Cancer|
|Subtitle of host publication||Mechanistic Aspects|
|Number of pages||17|
|State||Published - 1 Jan 2022|
- Oxidative stress