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Effects of intermittent hypoxia on the cell survival and inflammatory responses in the intertidal marine bivalves Mytilus edulis and Crassostrea gigas.

Hypoxia is a major stressor in estuarine and coastal habitats leading to adverse effects in aquatic organisms. Estuarine bivalves such as the blue mussels Mytilus edulis and the Pacific oysters Crassostrea gigas can survive periodic oxygen deficiency but the molecular mechanisms that underlie cellular injury during hypoxia-reoxygenation are not well understood. We examined the molecular markers of autophagy, apoptosis and inflammation during the short-term (1 day) and long-term (6 days) hypoxia and post-hypoxic recovery (1 h) in the mussels and oysters by measuring the lysosomal membrane stability, activity of a key autophagic enzyme (cathepsin D) and mRNA expression of the genes involved in the cellular survival and inflammation, including caspases 2, 3 and 8, Bcl-2, BAX, TGF-β-activated kinase 1 (TAK1), nuclear factor kappa B-1 (NF-κB), and NF-κB activating kinases IKKα and TBK1. C gigas exhibited higher hypoxia tolerance as well as blunted or delayed inflammatory and apoptotic response to hypoxia and reoxygenation shown by the later onset and/or the lack of transcriptional activation of caspases, BAX and an inflammatory effector NF-κB compared with M.edulis. Long-term hypoxia resulted in upregulation of Bcl-2 in the oysters and the mussels implying activation of the anti-apoptotic mechanisms. Our findings indicate the potential importance of the cell survival pathways in hypoxia tolerance of marine bivalves and demonstrate the utility of the molecular markers of apoptosis and autophagy for assessment of the sublethal hypoxic stress in bivalve populations.