Wounds cause more damage from oxidative stress (pink) in mice lacking peroxiredoxin 6 (right).
In vitro, Prdx6 neutralizes damaging reactive oxygen species (ROS). But scientists are just beginning to tease out its functions in vivo. Last year, the researchers found that rodents that overproduce Prdx6 in the skin suffer less damage from UV radiation. Moreover, the extra enzyme accelerates wound healing in aged animals, which are slow to mend. These results make sense, since sunburns induce ROS, and the inflammatory cells that arrive at an injury also spill the destructive molecules.
To further probe the enzyme's protective powers, the team gave Prdx6-deficient mice sunburns. The animals' keratinocytes, which normally divide rapidly to help restore the scorched skin, killed themselves in droves, suggesting that one of Prdx6's jobs is preventing damage to—and subsequent death of—repair cells. When the researchers sliced out patches of the rodents' skin, severe hemorrhages resulted. The new blood vessels sprouting into the cuts were flimsy because many of their endothelial cells were damaged or had committed suicide, the team found.
Vessel damage might occur because endothelial cells in Prdx6-deficient rodents can't fend off ROS or because inflammatory cells can't neutralize their own ROS, which then seep into the surrounding tissue. To test these alternatives, the researchers performed bone marrow transplants on normal mice and rodents lacking Prdx6.
Hemorrhages occurred when the recipient and the transferred cells were missing the enzyme. But some bleeding resulted when either the recipient animal or the implanted cells lacked Prdx6. Those results indicate that vessel weakness stems from lowered defenses in endothelial cells and from self-inflicted damage caused by ROS leakage from inflammatory cells. The findings also suggest that Prdx6 activators might help protect our skin from sun damage and even stave off skin cancer. 
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