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Cadmium adaptation in the lung - a double-edged sword?
B A Hart1, R J Potts, R D Watkin
1Department of Biochemistry, C-440 Given Medical Building, University of Vermont College of Medicine, Burlington, VT 05405, USA. bhart@zoo.uvm.edu
Toxicology
|March 14, 2001
Summary
Cadmium (Cd) adaptation in lungs enhances antioxidant defenses but impairs DNA repair and apoptosis. This adaptive response paradoxically promotes Cd carcinogenesis by allowing damaged cells to survive and proliferate.
Area of Science:
- Pulmonary toxicology
- Carcinogenesis
- Cellular adaptation
Background:
- Cadmium (Cd) exposure induces pulmonary adaptive responses.
- These adaptations include cellular proliferation and enhanced antioxidant defenses.
Purpose of the Study:
- To review cellular and molecular mechanisms of pulmonary adaptation to cadmium.
- To explore how these adaptations contribute to cadmium-induced carcinogenesis.
Main Methods:
- Review of existing literature on cellular and molecular responses to cadmium.
- Analysis of adaptive mechanisms including metallothionein and glutathione pathways.
- Examination of DNA repair and apoptosis in cadmium-adapted cells.
Main Results:
- Cadmium adaptation involves hyperplasia, hypertrophy, inflammation, and increased resistance factors like metallothionein and glutathione.
- Adapted cells show reduced DNA repair due to inhibited base excision repair enzymes.
- Apoptosis is attenuated in cadmium-adapted cells, promoting survival of damaged cells.
Conclusions:
- Pulmonary adaptation to cadmium is a double-edged sword.
- Impaired DNA repair and suppressed apoptosis in adapted cells promote cadmium carcinogenesis.
- Enhanced antioxidant defenses may also contribute to tumor resistance to chemotherapy.