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Published on: June 28, 2024
Oxidative stress and chromium(VI) carcinogenesis
Hua Yao1, Lan Guo, Bing-Hua Jiang
1Graduate Center for Toxicology, College of Medicine, the University of Kentucky, Lexington, KY 40515, USA.
Hexavalent chromium (Cr(VI)) exposure causes cancer through reactive oxygen species. This review details Cr(VI)-induced oxidative stress, its link to key cellular pathways, and disease progression mechanisms.
Area of Science:
- Environmental Health
- Toxicology
- Molecular Biology
Background:
- Hexavalent chromium (Cr(VI)) compounds are recognized environmental and industrial carcinogens.
- The precise biological mechanisms underlying Cr(VI) exposure-induced diseases remain incompletely elucidated.
- Growing evidence links Cr(VI) exposure to increased reactive oxygen species (ROS) generation and carcinogenic effects.
Purpose of the Study:
- To consolidate current literature on Cr(VI)-induced ROS generation in diverse systems.
- To explore the relationship between Cr(VI)-induced oxidative stress and critical cellular signaling pathways.
- To review the impact of Cr(VI) on cell cycle regulation and apoptosis.
Main Methods:
- Literature review of Cr(VI) effects in chemical and biological systems.
- Analysis of studies investigating ROS generation.
- Examination of research on transcription factor activation (NF-kappaB, AP-1, p53, HIF-1).
Main Results:
- Cr(VI) exposure is consistently associated with increased ROS production.
- Cr(VI)-induced oxidative stress activates key transcription factors including NF-kappaB, AP-1, p53, and HIF-1.
- Cr(VI) influences cell cycle progression and can trigger apoptosis.
Conclusions:
- Cr(VI)-induced ROS generation is a significant factor in its carcinogenicity.
- Oxidative stress mediated by Cr(VI) impacts crucial cellular pathways involved in disease development.
- Understanding these mechanisms is vital for assessing Cr(VI) health risks.
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