Islamabad, Jan 5 : Oxidative stress
damages DNA. Researchers in the Vetsuisse Faculty have now decoded the mechanism
that repairs DNA damaged in this way.
This repair mechanism could lead
to less invasive approaches in cancer therapy and contribute to the development
of new tests for the early diagnosis of cancer.
Oxidative stress is the
cause of many serious diseases such as cancer, Alzheimer's, arteriosclerosis and
diabetes. It occurs when the body is exposed to excessive amounts of
electrically charged, aggressive oxygen compounds.
These are normally
produced during breathing and other metabolic processes, but also in the case of
ongoing stress, exposure to UV light or X-rays. If the oxidative stress is too
high, it overwhelms the body's natural defences. The aggressive oxygen compounds
destroy genetic material, resulting in what are referred to as harmful
8-oxo-guanine base mutations in the DNA.
DNA repair mechanism
decoded
Together with the University of Oxford, Enni Markkanen, a
veterinarian in the working group of Prof. Ulrich Hübscher from the Institute of
Veterinary Biochemistry and Molecular Biology at the University of Zurich has
decoded and characterized the repair mechanism for the mutated DNA bases.
This mechanism efficiently copies thousands of 8-oxo-guanines without
their harmful mutations, thus normally preventing the negative consequences of
8-oxo-guanine damage. In their study, published in "PNAS," the researchers
outline the detailed processes involved in the local and temporal coordination
of this repair mechanism. Prof. Ulrich Hübscher hopes that this basic research
can be used therapeutically.
"We expect that the DNA repair mechanism
discovered here will lead to less invasive approaches in cancer therapy and that
it will be possible to develop new clinical tests for the early detection of
certain types of cancer."
In cooperation with University Hospital
Zurich, a study is already underway that involves examining samples of different
types of cancer for the repair gene and its
regulation.
Ends/Newswire
SA/EN
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