Effects of hypoxia-reoxygenation on the bioenergetics and oxidative stress in the isolated mitochondria of the king scallop, Pecten maximus.

The king scallop (Pecten maximus) is a highly aerobic subtidal bivalve species vulnerable to fluctuations in oxygen availability. This study investigated the effects of short-term (15†min) and long-term (90†min) hypoxia-reoxygenation (H/R) stress on substrate-specific mitochondrial functions in the gill and digestive gland tissues of P. maximus, oxidizing substrates that engage mitochondrial Complex I (pyruvate, palmitate) and Complex II (succinate). Under normoxic conditions, scallop mitochondria preferentially oxidized pyruvate. H/R stress induced a significant decline in Complex I-driven ATP synthesis, increased proton leak and dysregulated fatty acid oxidation, indicating mitochondrial vulnerability to H/R stress. Following H/R, both tissues demonstrated a greater capacity for succinate oxidation than for Complex I substrates; however, long-term H/R exposure led to a reduction in respiratory coupling efficiency across all substrates. Notably, gill mitochondria exhibited more effective regulation of reactive oxygen species efflux and electron leak compared with digestive gland mitochondria under H/R stress. Despite these physiological changes, no evidence of oxidative damage was detected, suggesting the presence of a robust mitochondrial antioxidant defense. Collectively, these findings suggest that succinate oxidation plays an important role in stress recovery in P. maximus, providing insights into mitochondrial resilience and the management of oxidative stress during intermittent hypoxia.