Oxidative Stress and Inflammation Linked to Frameshift Mutations
By biotechdaily.com staff writers Posted on 21 November 2003
Cancer researchers have found that malondialdehyde, an endogenous product of oxidative stress,
induces sequence-dependent frameshift mutations and base pair substitutions in bacteria and in
mammalian cells and may play a role in the development of colorectal cancer in humans.
Malondialdehyde reacts with guanine to form the exocyclic adduct,
pyrimido[1,2-alpha]purin-10(3H)-one (M1G). Investigators at Vanderbilt University (Nashville, TN,
USA) constructed DNA molecules with M1G inserted at different positions in the nucleotide sequence.
These molecules were inserted into both Escherichia coli and mammalian COS-7 kidney cells. After the
cells divided, the DNA was recovered from the new cells and examined for mutations. The results,
published in the November 5, 2003, online edition of the Proceedings of the [U.S.] National Academy
of Sciences, revealed that M1G induced sequence-dependent frameshift mutations and base pair
substitutions in both the bacteria and the mammalian cells.
“A number of studies have implicated chronic inflammation in the development of cancers, but the
specific way that occurs is not clear,†explained senior author Dr. Lawrence J. Marnett, director
of the Hancock Research Center at Vanderbilt University. “These studies suggest a direct link
between oxidative stress, like that seen in chronic inflammation, and genetic mutations that cause
human disease.â€
Copyright © 2003 medinews.com. All rights reserved.
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