Accumulation of Gut Bacteria May Cause the Age-Related Decline of Anoxia Tolerance in Adult Drosophila melanogaster


Meeting Abstract

4-5  Thursday, Jan. 4 09:00 – 09:15  Accumulation of Gut Bacteria May Cause the Age-Related Decline of Anoxia Tolerance in Adult Drosophila melanogaster SARGENT, JC*; CAMPBELL, JB; HARRISON, JF; ASU; ASU; ASU jcsargen@asu.edu

Cell death occurring from anoxia is the major pathology during heart attack, stroke and multiple other diseases. Humans vary substantially in their ability to survive anoxia, especially across ages, and the basis to this variation is not well-understood. Drosophila melanogaster have similar metabolic pathways to humans but have much better capacities to tolerate anoxia, suggesting that understanding mechanisms of anoxia tolerance in flies may provide insight for the development of new medical treatments. We exposed adult Drosophila, ages 1, 3, 5, 7, 9, and 12 days old, to six hours of anoxia and assessed survival 24-hours post-treatment. Seventy-nine percent of adults one day past eclosion survived; while only 10% of twelve-day-old adults survived; thus Drosophila show age-related decline in anoxia tolerance like humans. 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 maintain cellular energetic status. The concentration of bacteria in the gut is known to increase strongly with age in Drosophila. To test whether declining anoxia tolerance might be due to this increasing bacterial load, we replaced their food daily, every third day, or every sixth day, allowing us to vary gut bacterial load from low to high, respectively. At 12 days of age, each treatment group was exposed to six hours of anoxia and assayed for gut bacterial load. Anoxia tolerance was strongly and negatively affected by bacterial load. These data suggest that increasing bacterial load may play an important role in the age-related decline of anoxia tolerance in Drosophila. This research was supported by NSF IOS 1256745 and the SOLUR program at ASU.

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