Meeting Abstract
Mitochondria play a central role in ATP provisioning, redox and Ca2+ homeostasis, cellular signaling and life death decisions of aerobic organisms. Animal mitochondria are extremely sensitive to fluctuating oxygen (O2 ) levels such as occur during tissue ischemia and/or environmental hypoxia. In hypoxia-sensitive organisms, hypoxia and especially post-hypoxic reoxygenation cause mitochondrial injury due to the elevated production of reactive oxygen species, Ca2+ overload and damage to the mitochondrial membranes and enzymes; yet many hypoxia-tolerant species (including intertidal invertebrates) can endure frequent hypoxia-reoxygenation due to the diurnal and/or tidal O2 cycles without apparent ill effects on mitochondrial integrity and function. The mechanisms of such exceptional mitochondrial robustness are not yet fully understood. I will discuss the mitochondrial responses to intermittent hypoxia in marine intertidal mollusks emphasizing the potentially adaptive functional and proteomic changes of the mitochondria as well as the modulation of cellular protection and stress response pathways (including antioxidant defense, autophagy and apoptosis) that might contribute to high tolerance to fluctuating O2 levels in these organisms. I will also discuss the current knowledge gaps with an outlook to future studies needed to shed light on mitochondrial adaptations to frequent oxygen fluctuations and evolution of metabolism in extremely variable environments as well as identify potential targets for future therapies to protect sensitive mammalian tissues from stress-induced injuries (e.g. during ischemia-reperfusion).
