Meeting Abstract

16.6  Thursday, Jan. 3  Anoxic tolerance and oxygen reperfusion damage in Drosophila LIGHTON, J.R.B.*; SCHILMAN, P.E.; Univ. of Nevada, Las Vegas; Univ. of California, San Diego lighton@sablesys.com

The deleterious effects of anoxia followed by reperfusion with oxygen in higher animals including mammals are well known. A convenient and genetically well characterized small-animal model that exhibits reproducible, quantifiable oxygen reperfusion damage is currently lacking. We describe the dynamics of whole-organism metabolic recovery from anoxia in an insect, Drosophila melanogaster, and report that damage caused by oxygen reperfusion can be quantified in a novel but straightforward way. We monitored CO2 emission (an index of mitochondrial activity) and water vapor output (an index of neuromuscular control of the spiracles, which are valves between the outside air and the insect�s tracheal system) during entry into, and recovery from, rapid-onset anoxia exposure with durations ranging from 7.5 to 120 minutes. Anoxia caused a brief peak of CO2 output followed by knock-out. Mitochondrial respiration ceased and the spiracle constrictor muscles relaxed, then re-contracted. Reperfusion to normoxia caused bimodal re-activation of mitochondrial respiration, and slow inactivation then re-activation of the spiracle constrictor muscles. After long anoxia durations bimodality of mitochondrial reactivation was reduced and re-activation of spiracular control was impaired. Repeated reperfusion followed by episodes of anoxia depressed mitochondrial respiration and damaged the spiracular control system in a dose-dependent fashion. This is the first time that oxygen reperfusion damage has been described and quantified in an insect. We suggest that D. melanogaster may serve as an excellent experimental model for studying the underlying biology and mechanisms of ischemia and reperfusion damage.