DNA Repair and Oxidative Stress

The DNA inside cells is under continuous attack from heat, radiation and oxygen and one response of the cell to this outside factors is oxidative stress, which represents an imbalance in cell metabolism and it is related to a sum of human diseases, but, as a recent study conducted by three research groups at Emory University School of Medicine found out, it is also the trigger mechanism behind the relocation of certain DNA repair enzymes to the part of the cell were they are needed. This new understanding of cell response to genetic damage could open a new path in developing new anti-cancer drugs that interfere with DNA repair.

The research was made on strands of yeast, genetically modified so that two different DNA repair enzymes appeared fluorescent. The cells were exposed to hydrogen peroxide (which causes oxidative stress) and other chemicals that cause DNA damage.

One of the enzymes emphasized was Ntg1, which, researchers found, moves to the nucleus of the mitochondria (a part of the cell that has its own DNA) depending on where the DNA damage is concentrated. Its relocation seems to depend on the attachment to a small protein, called SUMO. This protein could prove to be a target for anti-cancer drugs and it is currently studied by numerous research groups.

Paul Doetsch, PhD, professor of biochemistry, radiation oncology, and hematology and oncology at Emory stated that “The more we know about how cells respond to oxidative stress, the more chances there could be to influence those responses for diagnostic or therapeutic purposes.”