by Will SansomReactive oxygen species (ROS) are not the nicest customers. You wouldn’t want to meet up with them in a dark alley. Like molecular "pinballs," ROS collide with other molecules to cause damage that may accumulate over time in our tissues. This is thought to result in the negative manifestations of aging, including cancer and neurodegenerative disease.
The oxidative stress theory of aging is extremely hot in research circles today. First proposed in 1956 and supported by recent studies made possible by new lab technologies, this theory holds that aging results from protein, lipid and DNA damage caused by ROS.
A new mouse study by Barshop Institute researchers points to the promise of one antioxidant compound to potentially slow this destructive trend. The study by Christie Lew and Lisa Cortez, research associates in the laboratory of faculty member Yuji Ikeno, M.D., Ph.D., was presented at a major scientific meeting in California this summer.
The group studied effects of an antioxidant called thioredoxin 1 (Trx1). Mice generated to have more Trx1 activity showed signs of slower aging than mice with normal Trx1 activity. The Trx1-enhanced mice had lower incidences of visible tumor at 26 months of age than the other group. They also had less oxidative damage in the liver. At 32 months of age, 52 percent of the Trx1-enhanced mice were still alive, compared to just 27 percent of the regular mice.
"These results support the hypothesis that the overexpression of Trx1 plays a protective role against oxidative stress, and therefore may have an impact on aging and age-related diseases," Dr. Ikeno said. He credits his staff’s efforts and lauds Arlan G. Richardson, Ph.D., Barshop Institute director, for his continuous support of the project.
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