Metabolic Expenditure

Bayne, B. L.

doi:10.1016/b978-0-12-803472-9.00006-6

Cited by 14 publications

(18 citation statements)

References 345 publications

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“…This increase appears largely driven by improved capacity of the mitochondrial ETS to utilize succinate whereas the ability to oxidize NADH-linked substrates such as pyruvate is not affected. Succinate is a common anaerobic end product in marine bivalves that accumulates in high concentrations during hypoxia (Hochachka and Mustafa, 1972;Bayne, 2017). High succinate oxidation capacity might be metabolically beneficial during post-hypoxic recovery in mussels helping to generate ATP with a highly abundant substrate (succinate) and restore normal levels of metabolic intermediates.…”

Section: H/r Stress Improves Mitochondrial Efficiency and Suppresses Ros Formationmentioning

confidence: 99%

Intrinsic Mechanisms Underlying Hypoxia-Tolerant Mitochondrial Phenotype During Hypoxia-Reoxygenation Stress in a Marine Facultative Anaerobe, the Blue Mussel Mytilus edulis

et al. 2021

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Hypoxia is common in marine environments and a major stressor for marine organisms inhabiting benthic and intertidal zones. Several studies have explored the responses of these organisms to hypoxic stress at the whole organism level with a focus on energy metabolism and mitochondrial response, but the instrinsic mitochondrial responses that support the organelle’s function under hypoxia and reoxygenation (H/R) stress are not well understood. We studied the effects of acute H/R stress (10 min anoxia followed by 15 min reoxygenation) on mitochondrial respiration, production of reactive oxygen species (ROS) and posttranslational modifications (PTM) of the proteome in a marine facultative anaerobe, the blue mussel Mytilus edulis. The mussels’ mitochondria showed increased OXPHOS respiration and suppressed proton leak resulting in a higher coupling efficiency after H/R stress. ROS production decreased in both the resting (LEAK) and phosphorylating (OXPHOS) state indicating that M. edulis was able to prevent oxidative stress and mitochondrial damage during reoxygenation. Hypoxia did not lead to rearrangement of the mitochondrial supercomplexes but impacted the mitochondrial phosphoproteome including the proteins involved in OXPHOS, amino acid- and fatty acid catabolism, and protein quality control. This study indicates that mussels’ mitochondria possess intrinsic mechanisms (including regulation via reversible protein phosphorylation) that ensure high respiratory flux and mitigate oxidative damage during H/R stress and contribute to the hypoxia-tolerant mitochondrial phenotype of this metabolically plastic species.

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Section: H/r Stress Improves Mitochondrial Efficiency and Suppresses Ros Formationmentioning

confidence: 99%

Intrinsic Mechanisms Underlying Hypoxia-Tolerant Mitochondrial Phenotype During Hypoxia-Reoxygenation Stress in a Marine Facultative Anaerobe, the Blue Mussel Mytilus edulis

et al. 2021

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“…However, it is a timelimited situation that requires the return of oxygen for an organism to recover and complete its life cycle. Post-hypoxic reoxygenation presents additional problems to aerobic organisms because of the energy costs associated with reinstatement of cellular homeostasis and increased biosynthesis to replenish energy reserves (Bayne, 2017;Ellington, 1983;Lewis et al, 2007). Furthermore, reoxygenation can cause oxidative damage via a surge of reactive oxygen species (ROS) from the mitochondrial electron transport system (ETS) (Andrienko et al, 2017;Jastroch et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

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

Falfushynska

Piontkivska

Sokolova

2020

Journal of Experimental Biology

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Hypoxia is a major stressor in estuarine and coastal habitats, leading to adverse effects in aquatic organisms. Estuarine bivalves such as blue mussels (Mytilus edulis) and 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 short-term (1 day) and long-term (6 days) hypoxia and post-hypoxic recovery (1 h) in 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 caspase 2, 3 and 8, Bcl-2, BAX, TGF-β-activated kinase 1 (TAK1), nuclear factor kappa B1 (NF-κB) and NF-κB activating kinases IKKα and TBK1. Crassostrea gigas exhibited higher hypoxia tolerance, as well as blunted or delayed inflammatory and apoptotic response to hypoxia and reoxygenation as shown by the later onset and/or the lack of transcriptional activation of caspases, BAX and the inflammatory effector NF-κB, compared with M. edulis. Long-term hypoxia resulted in upregulation of Bcl-2 in the oysters and mussels, implying activation of 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 the assessment of sublethal hypoxic stress in bivalve populations.

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“…Prior to this study, however, it remained unclear how this species behaves under chronic anoxia, especially since it is metabolically well‐adapted to deal with such environmental disturbances (i.e., facultative anaerobes; Hammen 1969). Mill River oysters may have responded to anoxia by initially closing their valves, switching ATP production to anaerobic pathways, and subsequently re‐opening their valves on an occasional basis to release acidic end‐products of glycolysis and avoid self‐poisoning (Bayne 2017). Once glycolysis starts, end‐products such as succinate and propionate can accumulate quite rapidly (≈12 h) in oyster tissues (Michaelidis et al 2005), whereas the depletion of endogenous energy reserves may span over several months (Deslous‐Paoli and Héral 1988; Whyte et al 1990; Ren and Schiel 2008).…”

Section: Discussionmentioning

confidence: 99%

“…with Pascale Nerette, a veterinarian working for the Government of New Brunswick, Canada. Given that C. virginica are hypoxia‐tolerant and facultative anaerobes (Bayne 2017), the abrupt wide‐scale mortality was surprising. As such, the mass mortality event prompted concern from industry and a subsequent collaborative investigation into the cause of death was initiated.…”

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confidence: 99%

The killer within: Endogenous bacteria accelerate oyster mortality during sustained anoxia

Coffin

Clements

Comeau

et al. 2021

Limnology & Oceanography

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Sustained periods of anoxia, driven by eutrophication, threaten coastal marine systems and can lead to mass mortalities of even resilient animals such as bivalves. While mortality rates under anoxia are well-studied, the specific mechanism(s) of mortality are less clear. We used a suite of complementary techniques (LT50, histology, 16S rRNA amplicon sequencing, and valvometry) to show that the proliferation of anaerobic bacteria within eastern oysters (Crassostrea virginica) accelerates mortality rate under anoxic conditions. Manipulative laboratory experiments revealed that oyster survival under anoxic conditions was halved when bacteria were present compared to when they were excluded by the broad-spectrum antibiotic chloramphenicol. Histological assessments supported this mechanism and showed infiltration of bacteria in oysters that were not treated with antibiotics compared to a general lack of bacteria when oysters were treated with antibiotics. 16S rRNA amplicon sequencing failed to identify any particular genera of bacteria responsible for mortality, rather a diversity of endogenous anaerobic and/or sulfate-reducing bacteria were common among oysters. In addition, monitoring of oyster valve gaping behavior in the field revealed that oysters showed remarkable valve closure synchrony when first exposed to anoxia. However, oysters periodically opened throughout anoxia/hypoxia in both the lab and field, suggesting that the infiltration of exogenous bacteria from the environment may also influence mortality rates under natural settings. Coupled with previous studies, we posit that mass mortality events in a wide range of coastal bivalves are likely the result of co-morbidity from asphyxiation and bacterial processes.

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Metabolic Expenditure

Cited by 14 publications

References 345 publications

Intrinsic Mechanisms Underlying Hypoxia-Tolerant Mitochondrial Phenotype During Hypoxia-Reoxygenation Stress in a Marine Facultative Anaerobe, the Blue Mussel Mytilus edulis

Intrinsic Mechanisms Underlying Hypoxia-Tolerant Mitochondrial Phenotype During Hypoxia-Reoxygenation Stress in a Marine Facultative Anaerobe, the Blue Mussel Mytilus edulis

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

The killer within: Endogenous bacteria accelerate oyster mortality during sustained anoxia

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