Tissue and substrate-dependent mitochondrial responses to Hypoxia/Reoxygenation stress in marine bivalve Crassostrea gigas (Thunberg, 1793).

Abstract

Hypoxia is a major stressor for aquatic organisms. In organisms like the intertidal oyster Crassostrea gigas, adaptations to frequent fluctuations in oxygen levels require metabolic plasticity to maintain mitochondrial function and adjust to shifts in substrate availability. This study investigated the effects of acute and long term hypoxia-reoxygenation (H/R) stress (15 min and 90 min at ~0% O2 for acute and long term exposures, respectively, and 10 min reoxygenation) on respiration (Mo2) and reactive oxygen species (ROS) generation in the gill and digestive gland mitochondria of C. gigas respiring on different substrates (pyruvate, succinate, and palmitate). Oyster mitochondria showed high capacity for succinate oxidation under normoxia in both studied tissues. Mitochondrial responses to H/R stress strongly depended on the oxidized substrate, the activity state of mitochondria and the type of hypoxia exposure. In both tissues, oxidizing exposure to both H/R stress suppressed Mo2 and ROS generation in the resting (LEAK state) mitochondria oxidizing NADH-linked substrates (palmitate/pyruvate). However, after acute H/R stress, mitochondria in ADP-stimulated (OXPHOS) state increased ROS production despite suppressed oxygen consumption. In mitochondria oxidizing FADH2–linked substrate (succinate), acute H/R exposure strongly increased Mo2 and ROS in LEAK and OXPHOS states, whereas; ROS production after long term H/R exposure was similar to normoxic conditions despite Mo2 suppression. Suppressed ability to oxidize NADH-linked substrates indicates that mitochondrial Complex I might be the key target of H/R induced injury in oyster mitochondria, which can be partially offset by robust succinate oxidation capacity to support ATP production during frequent oxygen fluctuations.