Meeting Abstract
Marine bivalves are champions of hypoxia tolerance commonly exposed to hypoxia due to the tidal, diurnal and seasonal oxygen cycles. Mitochondria are a hub of hypoxic damage in sensitive species, and it remains unknown how mitochondrial functions are preserved during hypoxia-reoxygenation in mollusks. We found that hypoxia and reoxygenation stimulate activity of mitochondrial electron transport chain in a hypoxia tolerant species, clams Mercenaria mercenaria but lead to mitochondrial deterioration and loss of OXPHOS capacity in hypoxia sensitive scallops Argopecten irradians . Hypoxia-reoxygenation led to upregulation of the mitochondrial heat shock protein HSP60 indicating damage to mitochondrial proteins in scallops but not in clams. Activities of proteasome and mitochondrial Lon protease were suppressed and phosphorylation of the elongation factor 1α elevated during hypoxia in clams indicating downregulation of the protein turnover in hypoxia-tolerant species. Unlike scallops, clam mitochondria respired ~3 times faster with succinate than pyruvate and were less sensitive to accumulation of bicarbonate and low pH commonly occurring during hypoxia. Fast oxidation of succinate may allow for rapid generation of ATP and restoration of acid-base balance by removing accumulated succinate during post-hypoxic recovery in clams. Mitochondrial ROS production was significantly higher in clams than in scallops, but no oxidative damage to mitochondrial lipids was observed in either species indicating that oxidative stress plays no role in species-specific resilience to oxygen fluctuations. Thus, mitochondrial adaptations in hypoxia-tolerant mollusks involve high capacity to oxidize anaerobic end products, tolerance to bicarbonate and low pH, enhanced protein homeostasis and reduction of the protein turnover during hypoxia.
