Previous epidemiological data has suggested that dietary antioxidants play a protective role against cancer. This has led to the proposal that dietary supplementation with antioxidants, such as vitamin C, may be useful in disease prevention. However, vitamin C has proved to be ineffective in cancer chemoprevention studies.
In addition, concerns have been raised over potentially deleterious transition metal-ion-mediated pro-oxidant effects.
A team from the Center for Cancer Pharmacology, University of Pennsylvania, Philadelphia, USA, investigated this phenomenon, using in vitro studies.
|Vitamin C induces lipid hydroperoxides to degrade into genotoxins.|
The results of their study were reported in the latest issue of Science.
They found that vitamin C induces lipid hydroperoxide decomposition to DNA-reactive bifunctional electrophiles. The electrophiles identified were 4-oxo-2-nonenal, 4,5-epoxy-2(E)-decenal, and 4-hydroxy-2-nonenal.
The compound 4,5-epoxy-2(E)-decenal is a precursor of etheno-2'-deoxyadenosine, a highly mutagenic lesion found in human DNA.
Lipid hydroperoxides are compounds that are produced in the body from dietary fat.
Seon Hwa Lee, concluded on behalf of the group, "Vitamin-C-mediated formation of genotoxins from lipid hydroperoxides, in the absence of transition metal ions, could help explain its lack of efficacy as a cancer chemoprevention agent."