Post-traumatic osteoarthritis (PTOA) is common following joint injuries. Injury itself and its after effects are known to kill chondrocytes. A large factor in the death of chondrocytes following blunt impact during in vitro studies has been superoxide release. Recent studies have shown that treating the injury with antioxidants can decrease the effects of the injury and increase chondrocyte viability. Past studies in our lab involving rotenone, an electron transport chain inhibitor, have indicated that the initial wave of reactive oxygen species (ROS) is mostly produced by mitochondria. However, that study covered only the first hour post-impact and a longer timeline of ROS production must be established to optimize antioxidant treatment. To address this we used a superoxide probe, Dihydroethidium (DHE), and confocal microscopy to track ROS production in live bovine osteochondral explants at varying times post-impact. Based on previous studies showing the timing of cell death, we hypothesized that the mitochondrial ROS production would diminish between 6 and 24 hours after impact. More cells were producing ROS at 6 hours than at 24 hours.
Eric Reese, ’11 Des Moines, IA
Majors: Biology, Psychology
University of Iowa Hospitals and Clinics
Sponsor: Marty Condon