Meeting Abstract
P3.213 Sunday, Jan. 6 Atmospheric oxygen availability affects insect thermotolerance at upper lethal temperatures, but oxygen delivery is not limiting under normoxia DE LOS SANTOS, R; MCCUE, M.D.*; St. Mary’s University; St. Mary’s University mmccue1@stmarytx.edu
Most natural environments experience fluctuating temperatures that acutely affect an organism’s physiology and ultimately a species’ biogeographic distribution. A popular paradigm in ectotherm thermobiology posits that O2 delivery to tissues becomes limiting as body temperature increases and eventually causes death at upper lethal temperatures. Because of the limited direct, experimental evidence supporting this paradigm, we explored the effect of ambient oxygen availability on the thermotolerance of several thousand insects representing six species (Acheta domesticus, Hippodamia convergens, Gromphadorhina portentosa, Pogonomyrmex occidentalis, Tenebrio molitor, and Zophobus morio), four taxonomic orders (Blattodea, Coleoptera, Hymenoptera, and Orthoptera), and multiple life stages (e.g., adults vs. larvae or nymphs). Survival curves of insects exposed to temperatures predetermined to cause death within one hour under normoxic conditions (21% O2) were compared with survival curves measured under artificial oxygen conditions (0, 10, 35, and 95% O2). Kaplan-Meier Log Rank analyses followed by Holm-Sidak pairwise comparisons revealed that: 1) anoxia sharply diminished survival times in all groups studied, 2) thermotolerance under moderate hyperoxia (35% O2) was no different from moderate hypoxia (10% O2); 3) insects exposed to either moderate or extreme hyperoxia (95% O2) showed no improved performance and occasionally reduced thermotolerance, and 4) thermotolerance differed with body mass and developmental stage among conspecifics, but that larger individuals are no more likely to be limited by oxygen delivery than much smaller conspecifics. We conclude that some factor(s) separate from oxygen delivery (e.g. denaturing protein or genetic material, membrane degradation, hypercapnia, etc.) is responsible for death of insects at upper lethal temperatures.
