Abstract
Epidemiological evidence suggests that exposure to certain metals causes carcinogenesis. The mechanisms of metal-induced carcinogenesis have been pursued in chemical, biochemical, cellular, and animal models. Significant evidence has accumulated that oxidative stress may be a common pathway in cellular responses to exposure to different metals. For example, in the last few years evidence in support of a correlation between the generation of reactive oxygen species, DNA damage, tumor promotion, and arsenic exposure has strengthened. This article summarizes the current literature on metal-mediated oxidative stress, apoptosis, and their relation to metal-mediated carcinogenesis, concentrating on arsenic and chromium.
| Original language | English |
|---|---|
| Pages (from-to) | 582-593 |
| Number of pages | 12 |
| Journal | Free Radical Biology and Medicine |
| Volume | 37 |
| Issue number | 5 |
| DOIs | |
| State | Published - Sep 1 2004 |
Keywords
- APL - acute promyelocytic leukemia
- Apoptosis
- Arsenic
- Carcinogenesis
- Chromium
- DMS - meso-2,3- dimercaptosuccinic acid
- GPx - glutathione peroxidase
- GSH - glutathione
- HaCat - human keratinocyte cell line
- Oxidative stress
- Signal transduction
Fingerprint
Dive into the research topics of 'Oxidative stress and apoptosis in metal ion-induced carcinogenesis'. Together they form a unique fingerprint.Cite this
- APA
- Author
- BIBTEX
- Harvard
- Standard
- RIS
- Vancouver