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Formation of Covalent DNA Adducts by Enzymatically Activated Carcinogens and Drugs In Vitro and Their Determination by 32P-postlabeling
Published on: March 20, 2018
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Selenium modifies carcinogen metabolism by inhibiting enzyme induction.
A Dipple1, M A Pigott, J A Milner
1LBI-Basic Research Program, NCI-Frederick Cancer Research Facility, 21701, Frederick, MD.
Biological Trace Element Research
|November 21, 2013
Summary
Sodium selenite inhibits the DNA binding of the carcinogen 7,12-dimethylbenz[a]anthracene. This protective action occurs by reducing a specific carcinogenic metabolite through enzyme inhibition.
Area of Science:
- Biochemistry
- Toxicology
- Carcinogenesis
Background:
- Selenium compounds, including sodium selenite, demonstrate protective effects against cancer development in various biological systems.
- The carcinogen 7,12-dimethylbenz[a]anthracene (DMBA) poses a risk due to its interaction with DNA.
Purpose of the Study:
- To elucidate the mechanism by which sodium selenite inhibits the DNA binding of the carcinogen 7,12-dimethylbenz[a]anthracene.
- To investigate the role of specific metabolites in the carcinogenicity of DMBA and the inhibitory action of selenite.
Main Methods:
- Investigating the interaction between sodium selenite and the carcinogen 7,12-dimethylbenz[a]anthracene.
- Analyzing the formation of DMBA metabolites and their binding to DNA.
- Assessing the effect of selenite on the enzyme systems responsible for generating reactive DMBA metabolites.
Main Results:
- Sodium selenite was found to preferentially reduce the DNA binding of an anti-dihydrodiol epoxide metabolite of 7,12-dimethylbenz[a]anthracene.
- Selenite's inhibitory effect was attributed to suppressing the induction of the enzyme system that produces this specific reactive metabolite.
Conclusions:
- Sodium selenite confers protection against 7,12-dimethylbenz[a]anthracene-induced DNA damage by targeting a key carcinogenic metabolite.
- The findings highlight a specific molecular mechanism for selenium's chemopreventive action against polycyclic aromatic hydrocarbon carcinogens.
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