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Biologically active compounds from pharmaceuticals cause concern due to their common occurrence in water and sediments of urbanized coasts and potential threat to marine organisms. Atorvastatin (ATO), a globally prescribed drug, is environmentally stable and bioavailable to marine organisms; however, the physiological and toxic effects of this drug on ecologically important coastal species are yet to be elucidated. We studied the effect of ATO (˜1.2 μg L -1 ) on bioenergetics (including whole-organism and mitochondrial respiration, as well as tissue energy reserves and mRNA expression of genes involved in mitochondrial biogenesis and fatty acid metabolism in the gills and the digestive gland) of a keystone bivalve Mytulis edulis (the blue mussel) from the Baltic Sea. Xenobiotic detoxification systems including activity and mRNA expression of P-glycoprotein, and Phase I and II biotransformation enzymes (cytochrome P450 monooxygenase CYP1A and glutathione transferase, GST) were also assessed in the gill and digestive gland of the mussels. Exposure to ATO caused rapid uptake and biotransformation of the drug by the mussels. Standard metabolic rate of ATO-exposed mussels increased by 56% indicating higher maintenance costs, yet no changes were detected in the respiratory capacity of isolated mitochondria. ATO exposure led to ˜60% decrease in the lysosomal membrane stability of hemocytes and ˜3-fold decrease in the whole-organism P-glycoprotein-driven and diffusional efflux of xenobiotics indicating altered membrane properties. The digestive gland was a major target of ATO toxicity in the mussels. Exposure of mussels to ATO led to depletion of lipid, carbohydrate and protein pools, and suppressed transcription of key enzymes involved in mitochondrial biogenesis (peroxisome proliferator-activated receptor gamma coactivator 1-alpha PGC-1α) and fatty acid metabolism (acetyl-CoA carboxylase and CYP4Y1) in the digestive gland. No bioenergetic disturbances were observed in the gills of ATO-exposed mussels, and elevated GST activity indicated enhanced ATO detoxification in this tissue. These data demonstrate that ATO can act as a metabolic disruptor and chemosensitizer in keystone marine bivalves and warrant further investigations of statins as emerging pollutants of concern in coastal marine ecosystems., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Salinity is an important environmental factor affecting physiology of marine organisms. Osmoconformers such as marine mollusks maintain metabolic function despite changes of the osmolarity and composition of the cytosol during salinity shifts. Currently, metabolic responses to the salinity-induced changes of the intracellular milieu are not well understood. We studied the effects of osmolarity (450 vs. 900 mOsm) and compatible osmolytes (70-590 mM of taurine or betaine) on isolated gill mitochondria of a marine osmoconformer, the Pacific oyster Crassostrea gigas. Physiological concentrations of taurine enhanced mitochondrial ATP synthesis and electron transport system (ETS) capacity, increased mitochondrial coupling and stimulated the forward flux through the Complex I. Notably, the stimulatory effects of taurine were more pronounced at 900 mOsm compared to 450 mOsm. In contrast, betaine proportionally increased the rates of the mitochondrial proton leak, oxidative phosphorylation and ETS flux (with no net effect on the mitochondrial coupling) and suppressed the activity of cytochrome c oxidase in oyster mitochondria. However, the effective concentration of betaine (590 mM) was higher than typically found in bivalves, and thus betaine is not likely to affect oyster mitochondria under the physiological conditions in vivo. Our findings indicate that taurine may support the mitochondrial bioenergetics during hyperosmotic stress in oysters. Compatibility of taurine with the metabolic functions and its beneficial effects on mitochondria may have contributed to its broad distribution as an osmolyte in marine osmoconformers and might explain the earlier reports of the positive effects of taurine supplementation on energy metabolism of other organisms, including mammals., (Copyright © 2018 Elsevier B.V. and Mitochondria Research Society. All rights reserved.)

Bioturbation of sediments by burrowing organisms plays a key role in the functioning of coastal ecosystems. Burrowing is considered an energetically expensive activity, yet the energy costs of burrowing and the potential impacts of multiple stressors (such as salinity stress and wave action) on bioenergetics and burrowing performance of marine bioturbators are not well understood. We investigated the effects of mechanical disturbance and salinity stress on the burrowing behavior, aerobic capacity and energy expense of digging in a common marine bioturbator, the soft-shell clam Mya arenaria from the Baltic Sea (control salinity 15). Mya arenaria showed large individual variability in the burrowing efficiency, with an average of ∼7% of the body energy reserves used per burial. Clams with higher mitochondrial capacity and lower energy expenditure per burial showed higher endurance. Acclimation for 3-4 weeks to low (5) or fluctuating (5-15) salinity reduced the burrowing speed and the number of times the clams can rebury but did not affect the mitochondrial capacity of the whole body or the gill. Acclimation to the fluctuating salinity shifted the predominant fuel use for burrowing from proteins to lipids. Our data indicate that the reduced burrowing performance of clams under the salinity stress is not due to the limitations of energy availability or aerobic capacity but must involve other mechanisms (such as impaired muscle performance). The reduction in the burrowing capacity of clams due to salinity stress may have important implications for survival, activity and ecological functions of the clams in shallow coastal ecosystems., Competing Interests: Competing interestsThe authors declare no competing or financial interests., (© 2018. Published by The Company of Biologists Ltd.)

Fluctuations in oxygen (O2) concentrations represent a major challenge to aerobic organisms and can be extremely damaging to their mitochondria. Marine intertidal molluscs are well-adapted to frequent O2 fluctuations, yet it remains unknown how their mitochondrial functions are regulated to sustain energy metabolism and prevent cellular damage during hypoxia and reoxygenation (H/R). We used metabolic control analysis to investigate the mechanisms of mitochondrial responses to H/R stress (18 h at <0.1% O2 followed by 1 h of reoxygenation) using hypoxia-tolerant intertidal clams Mercenaria mercenaria and hypoxia-sensitive subtidal scallops Argopecten irradians as models. We also assessed H/R-induced changes in cellular energy balance, oxidative damage and unfolded protein response to determine the potential links between mitochondrial dysfunction and cellular injury. Mitochondrial responses to H/R in scallops strongly resembled those in other hypoxia-sensitive organisms. Exposure to hypoxia followed by reoxygenation led to a strong decrease in the substrate oxidation (SOX) and phosphorylation (PHOS) capacities as well as partial depolarization of mitochondria of scallops. Elevated mRNA expression of a reactive oxygen species-sensitive enzyme aconitase and Lon protease (responsible for degradation of oxidized mitochondrial proteins) during H/R stress was consistent with elevated levels of oxidative stress in mitochondria of scallops. In hypoxia-tolerant clams, mitochondrial SOX capacity was enhanced during hypoxia and continued rising during the first hour of reoxygenation. In both species, the mitochondrial PHOS capacity was suppressed during hypoxia, likely to prevent ATP wastage by the reverse action of FO,F1-ATPase. The PHOS capacity recovered after 1 h of reoxygenation in clams but not in scallops. Compared with scallops, clams showed a greater suppression of energy-consuming processes (such as protein turnover and ion transport) during hypoxia, indicated by inactivation of the translation initiation factor EIF-2α, suppression of 26S proteasome activity and a dramatic decrease in the activity of Na(+)/K(+)-ATPase. The steady-state levels of adenylates were preserved during H/R exposure and AMP-dependent protein kinase was not activated in either species, indicating that the H/R exposure did not lead to severe energy deficiency. Taken together, our findings suggest that mitochondrial reorganizations sustaining high oxidative phosphorylation flux during recovery, combined with the ability to suppress ATP-demanding cellular functions during hypoxia, may contribute to high resilience of clams to H/R stress and help maintain energy homeostasis during frequent H/R cycles in the intertidal zone., (© 2016. Published by The Company of Biologists Ltd.)

Marine organisms are exposed to periodical oxygen deficiency and pollution stress in estuarine and coastal zones which may strongly affect their performance and survival. We studied the combined effects of exposure to a common pollutant, cadmium (Cd), and intermittent anoxia on anaerobic metabolism, energy status and mRNA expression of 13 genes involved in and/or controlled by the hypoxia inducible factor-1 (HIF-1) pathway in hepatopancreas of an intertidal bivalve, the eastern oyster Crassostrea virginica. In control oysters, prolonged anoxia resulted in a selective suppression of nitric oxide synthase (NOS) and upregulation of cytochrome c oxidase subunit IV (COX4) while the levels of other transcripts remained unchanged. During post-anoxic recovery, mRNA expression of hypoxia inducible factor-1alpha (HIF-1alpha) was elevated, phosphoenolpyruvate carboxykinase (PEPCK), NOS and LON protease suppressed, and mRNA expression of other studied genes not changed. Notably, most of the key glycolytic genes that are stimulated by HIF-1 in mammals, either remained unchanged or were downregulated in anoxic oysters suggesting a different mechanism of molecular response to oxygen deficiency. Patterns of transcriptional response during anoxia and reoxygenation were significantly altered by Cd exposure in a gene-specific manner. Anaerobic metabolism (indicated by accumulation of l-alanine, succinate and acetate during anoxia) was also suppressed in Cd-exposed oysters. In control oysters, ATP turnover rate (M(ATP)) during anoxia was mostly sustained by anaerobic glycolysis with negligible contributions from ATP and PLA breakdown. In contrast, in Cd-exposed oysters ATP breakdown contributed significantly to anaerobic M(ATP). Thus, while control oysters could efficiently defend the ATP levels and tissue energy status during prolonged anoxia, Cd-exposed oysters experienced a disturbance in tissue energy balance indicated by the depletion of ATP, a rapid decline in adenylate energy charge and increase in ADP/ATP ratios. This energy deficiency combined with suppression of anaerobic metabolism may strongly affect performance and survival of oysters in polluted estuaries where metal pollution may co-occur with "dead zones"., (Copyright 2010 Elsevier B.V. All rights reserved.)

Organic UV filters have emerged as a new threat to marine organisms, but ecotoxicological studies have so far focused on only a few substances despite the chemical diversity of these synthetic sunscreen agents. Here we examined the responses of blue mussels Mytilus edulis to ensulizole, a non-lipophilic UV filter commonly found in the Baltic Sea. Mussels were exposed for three weeks to five ensulizole concentrations of 10, 102, 103, 104, and 105 ng/L. Stress on stress response was evaluated by subjecting mussels to air exposure. A battery of biomarkers related to detoxification and antioxidant defense, oxidative stress damage, energy reserves and metabolism, autophagy, apoptosis, inflammation, and DNA damage was measured in the gills and the digestive gland. In general, ensulizole affected the antioxidant response, energy storage, and cell death-related processes in mussel tissues. Mussels exposed to low, environmentally relevant concentrations of ensulizole had a shorter air survival time than the control. Ensulizole often showed the non-monotonic concentration-response curves, suggesting the complex effects of this UV filter at molecular, biochemical, and organismal levels. [Display omitted] • Ecotoxicological evaluation of sunscreen agent ensulizole in mussels. • Ensulizole reduces survival in air at environmentally relevant concentrations. • Ensulizole causes subcellular effects in the gills and digestive gland. • Ensulizole induces non-monotonic responses. [ABSTRACT FROM AUTHOR]