A powerful antioxidant known as MitoQ may be able to peel years off the arteries of individuals at risk for heart disease and prevent them from becoming more ill. Researchers at the University of Colorado Boulder conducted a study that administered MitoQ to old mice (~80 human years old), and the team discovered the antioxidant improved the function of the mouses’ arteries to those of young mice (~35 human years old). This special compound might now be implicated in further studies to develop it for clinical use to combat the increased risk for heart disease during aging.
“One of the hallmarks of primary aging is endothelial dysfunction,” said Rachel Gioscia-Ryan, who is lead author on the study published in The Journal of Physiology, in a news release from Boulder. “MitoQ completely restored endothelial function in the old mice. They looked like young mice.”
The team led by Gioscia-Ryan, a doctoral student, and her adviser, Professor Douglas Seals, was interested in using the mitochondria-targeted MitoQ due to its proposed benefits on the endothelium lining of blood vessels. In old age, nitric oxide that is produced in the endothelium to dilate the blood vessels is destroyed by reactive oxygen species (ROS) from the mitochondria. With less nitric oxide available for dilation, blood vessels have difficulty dilating when it is necessary, causing the heart to work harder to pump blood and increasing the risk for heart disease.
Normally, the balance between ROS and nitric oxide can be maintained by the body’s own antioxidants. However, in old age, the body produces more ROS than it can handle, leading to oxidative stress. “You have this kind of balance, but with aging there is this shift,” said Gioscia-Ryan. “There become way more ROS than your antioxidant defenses can handle.” As a mitochondria-targeted antioxidant, MitoQ was hypothesized to help.
In Gioscia-Ryan and Dr. Seals’ study, “Mitochondria-targeted Antioxidant (MitoQ) Ameliorates Age-related Arterial Endothelial Dysfunction in Mice,” the research team at Boulder administered MitoQ to mice via drinking water for four weeks to see if endothelium-dependent dilation (EDD) would improve as a result of increased nitric oxide bioavailability. When conducting tests after the four-week treatment period, the team identified a more normal level of mitochondria-derived ROS and an increase in vascular mitochondrial health.
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