Defense Capacities Against Oxidative Stress in Diapause and Post-Diapause Embryos of Artemia franciscana

Embryos of Artemia franciscana survive harsh conditions in diapause and anoxia-induced quiescence for years by undergoing deep metabolic transitions. During reactivation of metabolism, both the release of reactive oxygen species (ROS) from mitochondria and oxidative damage in mitochondria are low compared to mammalian mitochondria. Because antioxidant pathways can be important for avoiding oxidative stress upon metabolic reactivation in some cases, part of the low ROS efflux from A. franciscana mitochondria could be attributed to scavenging. Consequently, we analyzed activities of antioxidant enzymes and quantities of small-molecule antioxidants in diapause versus post-diapause embryos under steady-state conditions. Functional capacities of most antioxidant enzymes (total superoxide dismutase [Cu/Zn-SOD + Mn-SOD], Mn-SOD, and glutathione reductase [GR]) were higher in the post-diapause state. These changes are understandable based on very elevated metabolic rates during post-diapause, and the correspondingly higher defense capacities necessitated against ROS. Conversely, quantities of reduced glutathione (GSH), along with the total GSH pool (GSH + GSSG), were higher during diapause. The depressed metabolic rates during diapause predictably foster lower ROS generation (oxidative stress) to impact the GSH pool, so the standing quantity of reduced species in the pool is greater. However, our literature survey suggests that, overall, A. franciscana embryos do not possess abnormally elevated defenses against oxidative stress when compared to other hypoxia/anoxia-tolerant species or even intolerant species. Thus, avoiding the actual generation of large ROS bursts after metabolic reactivation appears to be the more important contributor to protection of the embryos compared to ROS scavenging per se.