Meeting Abstract
Cell death occurring from anoxia is considered to be the major pathology for many human diseases such as heart attack and stroke. Though much is known about the cause of anoxia in such conditions, we still have a poor understanding of the mechanisms causing cell death and the genetic and physiological processes responsible for variation in survival of anoxia. Drosophila melanogaster are particularly interesting models for studying responses to anoxia as they can survive many hours of anoxia and most of their metabolic pathways are similar to those of humans. Based on studies with humans, we hypothesized that younger adults would have a higher anoxia tolerance than older adults. We exposed adult Drosophila, ages 1, 3, 5, 7, 9, and 12 days old, to six hours of anoxia. Survival was assessed 24 hours post-treatment and declined with age in a linear fashion for females and in a more exponential fashion for males. Seventy nine percent of adults one day past eclosion survived six hours of anoxia; while only 10% of twelve-day-old adults survived. Additionally, we measured ATP in 1 and 12 day old Drosophila in different durations of anoxia. In anoxia, ATP levels declined rapidly (< 30 min) to near-zero levels in both 1 and 12 day old adults; thus the better anoxia-tolerance of young adults is not due to a better capacity to keep ATP elevated. This age-related decline in anoxia tolerance may be due to loss of capacities to prevent or repair anoxia-related damage. Overall, these data show that patterns of gender- and age-associated variation in tolerance to anoxia are similar in Drosophila and mammals, suggesting that Drosophila may be underutilized models for studies of the genetic and biochemical mechanisms of pathology of stroke and heart disease. This research was partially supported by NSF IOS 1256745.
