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.

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