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Carcinogenic metals and NF-kappaB activation.
1Health Effects Laboratory Division, National Institute for Occupational State and Health, Morgantown, WV 26505, USA.
Molecular and Cellular Biochemistry
|October 27, 2001
Summary
Certain metals like chromium and arsenic are carcinogenic. This review explores how these metals trigger cellular signals, like reactive oxygen species (ROS), and activate NF-kappaB, a key factor in disease development.
Area of Science:
- Environmental Toxicology
- Molecular Carcinogenesis
- Signal Transduction
Background:
- Epidemiological and animal studies link several metals (e.g., chromium, arsenic, vanadium, nickel) to mutagenicity and carcinogenicity.
- Decades of research have elucidated metal-induced pathophysiological processes at chemical and cellular levels.
- Carcinogenic metals, despite unique mechanisms, may share common signaling molecules like reactive oxygen species (ROS).
Purpose of the Study:
- To review the molecular mechanisms of metal-induced carcinogenesis.
- To focus on signal transduction pathways activated by carcinogenic metals.
- To highlight the role of NF-kappaB activation in metal-induced diseases.
Main Methods:
- Review of epidemiological, animal, chemical, and cellular studies.
- Analysis of recent advancements in molecular carcinogenesis techniques.
- Focus on signal transduction pathways and transcription factor activation.
Main Results:
- Metals like chromium, arsenic, vanadium, and nickel are identified as potent mutagens and carcinogens.
- Reactive oxygen species (ROS) are implicated as common signaling molecules in metal-induced carcinogenesis.
- Metal exposure activates specific signal transduction pathways, leading to NF-kappaB activation.
Conclusions:
- Carcinogenic metals disrupt cellular signaling, contributing to disease.
- Activation of NF-kappaB by metals is a critical step in the development of various human diseases.
- Understanding these molecular mechanisms is crucial for developing preventative and therapeutic strategies against metal-induced pathologies.
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