In mammals, much of the damage that occurs in the heart after oxygen deprivation is caused by the return of oxygen to the tissue. “When oxygen returns, toxic reactive oxygen species (ROS) are produced in the mitochondria,” said Amanda Bundgård, a PhD candidate and lead author on the study. Turtles have been suggested as a good model animal to study aging because they live remarkably long lives with relatively low age-related deterioration (senescence).
“We investigated whether turtles may avoid oxidative damage in the heart after winter hibernation by specifically inhibiting the mitochondrial protein complex I, which is responsible for the production of ROS,” Bundgård explained. “We found that, although complex I inhibition was a potent means to prevent ROS in the heart, this was apparently not the turtle’s main strategy to prevent oxidative stress after the absence of oxygen (anoxia). Instead, turtles seem to rely on a general suppression of mitochondrial function, whose mechanisms we still need to understand, but that may fit well with the already low metabolic rates of turtles compared to mammals.”
The research team found that reducing the content of mitochondria in the turtle heart during prolonged anoxia may prevent ROS production upon reoxygenation and protect against oxidative damage. “It is possible that the remarkable ability of freshwater turtles to survive oxygen deficiency for months may in part rely on some mitochondrial shutdown, which is something we may one day be able to exploit to protect the sensitive mammalian heart from oxidative damage following a heart attack,” Bundgård said. “Whether this mitochondrial inhibition happens naturally in the turtle during anoxia has not actually been investigated directly and is our next step in this study.”
Amanda Bundgård will present “Mitochondrial regulation protects the turtle heart from oxidative damage after reoxygenation” at a poster session on Monday, August 28, from 5 to 7 p.m. in the U.S. Grant Hotel.