Anoxia is the condition of extreme oxygen deprivation. It presents real danger to the viability of tissues, subjected to inadequate oxygen supply. Different organisms have various degrees of susceptibility to anoxic stress conditions. Thousands of human deaths each year are attributed to the events of induced anoxic conditions – ischemic strokes and heart attacks being one the most numerous. But whereas mammals tolerate anoxic stress very poorly, D. melanogaster is known to develop a special protective mechanism – spreading depression, allowing it to withstand hours of oxygen deprivation. Period following reintroduction of oxygen is the most dangerous consequence of anoxia and is characterized by the abundance of ROS (Reactive Oxygen Species), which oxidize vital molecules in cells rendering them non-functional. Methionine is exceptionally susceptible to oxidation by ROS, but it can be catalytically restored by the enzyme Methionine Sulfoxide Reductase (Msr). Two forms of Msr are known – MsrA and MsrB, which act upon two different epimers of oxidized methionine. Currently, little is known of the relationship between Msr gene activity and anoxic stress recovery in Drosophila. Activity of the Msr-encoding genes in response to anoxia is the subject of the proposed study. We use anoxia chamber to induce comma in flies, followed by recording recovery times. Preliminary results show, that single mutant flies do not take significantly longer than wildtype to recover from spreading depression. However, double mutants take significantly longer to recover and greater number of Msr-deficient flies die as a result of anoxia. Failure to recover becomes more pronounced as animals approach senescence. These studies offer insight into the role of oxidative damage during reperfusion period following cardiac stroke.