This content is adapted from an article on www.cosmeticsandtoiletries.com.
Free radicals might not be all bad, according to researchers from the University of California, San Diego. Andrew Chishold, PhD, and his fellow researchers found reactive oxygen species (ROS) to be beneficial to wound healing.
In an October 13, 2014 Developmental Cell article, the researchers found a cytoprotective role of mitochondrial ROS (mtROS) in Caenorhabditis elegans skin wound healing. Of course, the research was conducted on laboratory roundworms; however, the researchers are confident the results will translate to larger animals, as ROS-like superoxides have been observed at skin wound sites.
Skin wounding causes local production of mtROS superoxide at the wound site. Inhibition of mtROS levels by mitochondrial superoxide-specific antioxidants blocks actin-based wound closure, whereas elevation of mtROS promotes wound closure and enhances survival of mutant animals defective in wound healing.
mtROS act downstream of wound-triggered Ca2+ influx. The researchers revealed that the mitochondrial calcium uniporter MCU-1 is essential for rapid mitochondrial Ca2+ uptake and mtROS production after wounding. mtROS can promote wound closure by local inhibition of Rho GTPase activity via a redox-sensitive motif.
Therefore, while too much ROS in the cell may be bad, eliminating ROS altogether may prevent wound healing. The researchers have future plans to conduct the experiment on rodents.
