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DOE OSTI2020

Acidification in the U.S. Southeast: Causes, Potential Consequences and the Role of the Southeast Ocean and Coastal Acidification Network

Coastal acidification in southeastern U.S. estuaries and coastal waters is influenced by biological activity, run-off from the land, and increasing carbon dioxide in the atmosphere. Acidification can negatively impact coastal resources such as shellfish, finfish, and coral reefs, and the communities that rely on them. Organismal responses for species located in the U.S. Southeast document large negative impacts of acidification, especially in larval stages. For example, the toxicity of pesticides increases under acidified conditions and the combination of acidification and low oxygen has profoundly negative influences on genes regulating oxygen consumption. In corals, the rate of calcification decreases with acidification and processes such as wound recovery, reproduction, and recruitment are negatively impacted. Minimizing the changes in global ocean chemistry will ultimately depend on the reduction of carbon dioxide emissions, but adaptation to these changes and mitigation of the local stressors that exacerbate global acidification can be addressed locally. The evolution of our knowledge of acidification, from basic understanding of the problem to the emergence of applied research and monitoring, has been facilitated by the development of regional Coastal Acidification Networks (CANs) across the United States. This synthesis is a product of the Southeast Coastal and Ocean Acidification Network (SOCAN). SOCAN was established to better understand acidification in the coastal waters of the U.S. Southeast and to foster communication among scientists, resource managers, businesses, and governments in the region. Here we review acidification issues in the U.S. Southeast, including the regional mechanisms of acidification and their potential impacts on biological resources and coastal communities. We recommend research and monitoring priorities and discuss the role SOCAN has in advancing acidification research and mitigation of and adaptation to these changes.

54 ENVIRONMENTAL SCIENCES↗

DOE OSTI2016

Ocean acidification over the next three centuries using a simple global climate carbon-cycle model: projections and sensitivities

Continued oceanic uptake of anthropogenic CO 2 is projected to significantly alter the chemistry of the upper oceans over the next three centuries, with potentially serious consequences for marine ecosystems. Relatively few models have the capability to make projections of ocean acidification, limiting our ability to assess the impacts and probabilities of ocean changes. In this study we examine the ability of Hector v1.1, a reduced-form global model, to project changes in the upper ocean carbonate system over the next three centuries, and quantify the model's sensitivity to parametric inputs. Hector is run under prescribed emission pathways from the Representative Concentration Pathways (RCPs) and compared to both observations and a suite of Coupled Model Intercomparison (CMIP5) model outputs. Current observations confirm that ocean acidification is already taking place, and CMIP5 models project significant changes occurring to 2300. Hector is consistent with the observational record within both the high- (> 55°) and low-latitude oceans (< 55°). The model projects low-latitude surface ocean pH to decrease from preindustrial levels of 8.17 to 7.77 in 2100, and to 7.50 in 2300; aragonite saturation levels (Ω Ar ) decrease from 4.1 units to 2.2 in 2100 and 1.4 in 2300 under RCP 8.5. These magnitudes and trends of ocean acidification within Hector are largely consistent with the CMIP5 model outputs, although we identify some small biases within Hector's carbonate system. Of the parameters tested, changes in [H + ] are most sensitive to parameters that directly affect atmospheric CO 2 concentrations – Q 10 (terrestrial respiration temperature response) as well as changes in ocean circulation, while changes in Ω Ar saturation levels are sensitive to changes in ocean salinity and Q 10 . We conclude that Hector is a robust tool well suited for rapid ocean acidification projections and sensitivity analyses, and it is capable of emulating both current observations and large-scale climate models under multiple emission pathways.

54 ENVIRONMENTAL SCIENCES↗

DOE OSTI2018

Climate Change Impacts on Natural Sulfur Production: Ocean Acidification and Community Shifts

Utilizing the reduced-complexity model Hector, a regional scale analysis was conducted quantifying the possible effects climate change may have on dimethyl sulfide (DMS) emissions within the oceans. The investigation began with a review of the sulfur cycle in modern Earth system models. We then expanded the biogeochemical representation within Hector to include a natural ocean component while accounting for acidification and planktonic community shifts. The report presents results from both a latitudinal and a global perspective. This new approach highlights disparate outcomes which have been inadequately characterized via planetary averages in past publications. Our findings suggest that natural sulfur emissions (ESN) may exert a forcing up to 4 times that of the CO 2 marine feedback, 0.62 and 0.15 Wm –2 , respectively, and reverse the radiative forcing sign in low latitudes. Additionally, sensitivity tests were conducted to demonstrate the need for further examination of the DMS loop. As a result, the present work attempts to include dynamic ESN within reduced-complexity simulations of the sulfur cycle, illustrating its impact on the global radiative budget.

54 ENVIRONMENTAL SCIENCES↗

DOE OSTI2015

Extracellular acidification synergizes with PDGF to stimulate migration of mouse embryo fibroblasts through activation of p38MAPK with a PTX-sensitive manner

The elucidation of the functional mechanisms of extracellular acidification stimulating intracellular signaling pathway is of great importance for developing new targets of treatment for solid tumors, and inflammatory disorders characterized by extracellular acidification. In the present study, we focus on the regulation of extracellular acidification on intracellular signaling pathways in mouse embryo fibroblasts (MEFs). We found extracellular acidification was at least partly involved in stimulating p38MAPK pathway through PTX-sensitive behavior to enhance cell migration in the presence or absence of platelet-derived growth factor (PDGF). Statistical analysis showed that the actions of extracellular acidic pH and PDGF on inducing enhancement of cell migration were not an additive effect. However, we also found extracellular acidic pH did inhibit the viability and proliferation of MEFs, suggesting that extracellular acidification stimulates cell migration probably through proton-sensing mechanisms within MEFs. Using OGR1-, GPR4-, and TDAG8-gene knock out technology, and real-time qPCR, we found known proton-sensing G protein-coupled receptors (GPCRs), transient receptor potential vanilloid subtype 1 (TRPV1), and acid-sensing ion channels (ASICs) were unlikely to be involved in the regulation of acidification on cell migration. In conclusion, our present study validates that extracellular acidification stimulates chemotactic migration of MEFs through activation of p38MAPK with a PTX-sensitive mechanism either by itself, or synergistically with PDGF, which was not regulated by the known proton-sensing GPCRs, TRPV1, or ASICs. Our results suggested that others proton-sensing GPCRs or ion channels might exist in MEFs, which mediates cell migration induced by extracellular acidification in the presence or absence of PDGF. - Highlights: • Acidic pH and PDGF synergize to stimulate MEFs migration via Gi/p38MAPK pathway. • Extracellular acidification inhibits the viability and proliferation of MEFs. • MEFs sense acidic pH was not regulated by known proton-sensing GPCRs, TRPV1 or ASICs.

60 APPLIED LIFE SCIENCES↗

DOE OSTI2018

Combined effects of warming and acidification on accumulation and elimination dynamics of paralytic shellfish toxins in mussels Mytilus galloprovincialis

Highlights: • Impact of warming and acidification on the accumulation/elimination dynamics of HAB-toxins in shellfish. • High toxicity levels were found under current conditions. • Climate change scenarios may lead to lower but prolonged PST contamination. Harmful algal blooms (HAB) have been increasing in frequency and intensity most likely due to changes on global conditions, which constitute a significant threat to wild shellfish and its commercial farming. This study evaluated the impact of increasing seawater temperature and acidification on the accumulation/elimination dynamics of HAB-toxins in shellfish. Mytilus galloprovincialis were acclimated to four environmental conditions simulating different climate change scenarios: i) current conditions, ii) warming, iii) acidification and iv) interaction of warming with acidification. Once acclimated, mussels were exposed to the paralytic shellfish toxins (PSTs) producing dinoflagellate Gymnodinium catenatum for 5 days and to non-toxic diet during the subsequent 10 days. High toxicity levels (1493 µg STX eq. kg{sup −1}) exceeding the safety limits were determined under current conditions at the end of the uptake period. Significantly lower PSP toxicity levels were registered for warming- and acidification-acclimated mussels (661 and 761 µg STX eq. kg{sup −1}). The combined effect of both warming and acidification resulted in PSP toxicity values slightly higher (856 μg STX eq. kg{sup −1}). A rapid decrease of toxicity was observed in mussels at the current conditions after shifting to a non-toxic diet, which was not noticed under the predicted climate change scenarios. Variability of each PST analogue, measured throughout the experiment, highlighted different mechanisms are associated with changes of each environmental factor, although both resulting in lower toxicity. Warming-acclimated mussels showed lower accumulation/elimination rates, while acidification-acclimated mussels showed higher capability to accumulate toxins, but also a higher elimination rate preventing high toxicity levels. As different mechanisms are triggered by warming and acidification, their combined effect not leads to a synergism of their individual effects. The present work is the first assessing the combined effect of climate change drivers on accumulation/elimination of PSTs, in mussels, indicating that warming and acidification may lead to lower toxicity values but longer toxic episodes. PSTs are responsible for the food poisoning syndrome, paralytic shellfish poisoning (PSP) in humans. This study can be considered as the first step to build models for predicting shellfish toxicity under climate change scenarios.

54 ENVIRONMENTAL SCIENCES↗

DOE OSTI2011

Extracellular acidification induces connective tissue growth factor production through proton-sensing receptor OGR1 in human airway smooth muscle cells

Highlights: {yields} The involvement of extracellular acidification in airway remodeling was investigated. {yields} Extracellular acidification alone induced CTGF production in human ASMCs. {yields} Extracellular acidification enhanced TGF-{beta}-induced CTGF production in human ASMCs. {yields} Proton-sensing receptor OGR1 was involved in acidic pH-stimulated CTGF production. {yields} OGR1 may play an important role in airway remodeling in asthma. -- Abstract: Asthma is characterized by airway inflammation, hyper-responsiveness and remodeling. Extracellular acidification is known to be associated with severe asthma; however, the role of extracellular acidification in airway remodeling remains elusive. In the present study, the effects of acidification on the expression of connective tissue growth factor (CTGF), a critical factor involved in the formation of extracellular matrix proteins and hence airway remodeling, were examined in human airway smooth muscle cells (ASMCs). Acidic pH alone induced a substantial production of CTGF, and enhanced transforming growth factor (TGF)-{beta}-induced CTGF mRNA and protein expression. The extracellular acidic pH-induced effects were inhibited by knockdown of a proton-sensing ovarian cancer G-protein-coupled receptor (OGR1) with its specific small interfering RNA and by addition of the G{sub q/11} protein-specific inhibitor, YM-254890, or the inositol-1,4,5-trisphosphate (IP{sub 3}) receptor antagonist, 2-APB. In conclusion, extracellular acidification induces CTGF production through the OGR1/G{sub q/11} protein and inositol-1,4,5-trisphosphate-induced Ca{sup 2+} mobilization in human ASMCs.

60 APPLIED LIFE SCIENCES↗

DOE OSTI2012

Moderate extracellular acidification inhibits capsaicin-induced cell death through regulating calcium mobilization, NF-{kappa}B translocation and ROS production in synoviocytes

Highlights: Black-Right-Pointing-Pointer Moderate extracellular acidification regulates intracellular Ca{sup 2+} mobilization. Black-Right-Pointing-Pointer Moderate acidification activates NF-{kappa}B nuclear translocation in synoviocytes. Black-Right-Pointing-Pointer Moderate acidification depresses the ROS production induced by capsaicin. Black-Right-Pointing-Pointer Moderate acidification inhibits capsaicin-caused synoviocyte death. -- Abstract: We previously show the expression of transient receptor potential vanilloid 1 (TRPV1) in primary synoviocytes from collagen-induced arthritis (CIA) rats. Capsaicin and lowered extracellular pH from 7.4 to 5.5 induce cell death through TRPV1-mediated Ca{sup 2+} entry and reactive oxygen species (ROS) production. However, under the pathological condition in rheumatoid arthritis, the synovial fluid is acidified to a moderate level (about pH 6.8). In the present study, we examined the effects of pH 6.8 on the TRPV1-mediated cell death. Our finding is different or even opposite from what was observed at pH 5.5. We found that the moderate extracellular acidification (from pH 7.4 to 6.8) inhibited the capsaicin-induced Ca{sup 2+} entry through attenuating the activity of TRPV1. In the mean time, it triggered a phospholipse C (PLC)-related Ca{sup 2+} release from intracellular stores. The nuclear translocation of NF-{kappa}B was found at pH 6.8, and this also depends on PLC activation. Moreover, the capsaicin-evoked massive ROS production and cell death were depressed at pH 6.8, both of which are dependent on the activation of PLC and NF-{kappa}B. Taken together, these results suggested that the moderate extracellular acidification inhibited the capsaicin-induced synoviocyte death through regulating Ca{sup 2+} mobilization, activating NF-{kappa}B nuclear translocation and depressing ROS production.

60 APPLIED LIFE SCIENCES↗

DOE OSTI2016

Inhibition of mTOR improves the impairment of acidification in autophagic vesicles caused by hepatic steatosis

Recent investigations revealed that dysfunction of autophagy involved in the progression of chronic liver diseases such as alcoholic and nonalcoholic steatohepatitis and hepatocellular neoplasia. Previously, it was reported that hepatic steatosis disturbs autophagic proteolysis via suppression of both autophagic induction and lysosomal function. Here, we demonstrate that autophagic acidification was altered by a decrease in lysosomal proton pump vacuolar-ATPase (V-ATPase) in steatohepatitis. The number of autophagic vesicles was increased in hepatocytes from obese KKAy mice as compared to control. Similarly, autophagic membrane protein LC3-II and lysosomal protein LAMP-2 expression were enhanced in KKAy mice liver. Nevertheless, both phospho-mTOR and p62 expression were augmented in KKAy mice liver. More than 70% of autophagosomes were stained by LysoTracker Red (LTR) in hepatocytes from control mice; however, the percentage of acidic autolysosomes was decreased in hepatocytes from KKAy mice significantly (40.1 ± 3.48%). Both protein and RNA level of V-ATPase subunits ATP6v1a, ATP6v1b, ATP6v1d in isolated lysosomes were suppressed in KKAy mice as compared to control. Interestingly, incubation with mTOR inhibitor rapamycin increased in the rate of LTR-positive autolysosomes in hepatocytes from KKAy mice and suppressed p62 accumulation in the liver from KKAy mice which correlated to an increase in the V-ATPase subunits expression. These results indicate that down-regulation of V-ATPase due to hepatic steatosis causes autophagic dysfunction via disruption of lysosomal and autophagic acidification. Moreover, activation of mTOR plays a pivotal role on dysregulation of lysosomal and autophagic acidification by modulation of V-ATPase expression and could therefore be a useful therapeutic target to ameliorate dysfunction of autophagy in NAFLD. - Highlights: • Hepatic steatosis causes accumulation of autophagic vesicles in hepatocytes. • Hepatic steatosis disturbs acidification of autophagic vesicles. • Lipid accumulation suppresses the expression of lysosomal V-ATPase subunits. • Rapamycin upregulates the expression of lysosomal V-ATPase suppressed in NAFLD. • Rapamycin ameliorates the acidification of autolysosomes impaired in NAFLD.

60 APPLIED LIFE SCIENCES↗

DOE OSTI2021

Evaluating bloom potential of the green-tide forming alga Ulva ohnoi under ocean acidification and warming

Herein we discuss the occurrence of green-tides, whose bloom potential may be increased by various human activities and biogeochemical process, results in enormous economic losses and ecosystem collapse. In this study, we investigated the ecophysiology of the subtropical green-tide forming alga, Ulva ohnoi complex (hereafter: U. ohnoi), under simulated future ocean conditions in order to predict its bloom potential using photosynthesis and growth measurements, and stable isotope analyses. Our mesocosm system included four experimental conditions that simulated the individual and combined effects of elevated CO 2 and temperature, namely control (450 μatm CO 2 & 20 °C), acidification (900 μatm CO 2 & 20 °C), warming (450 μatm CO 2 & 25 °C), and greenhouse (900 μatm CO 2 & 25 °C). Photosynthetic electron transport rates (rETR) increased significantly under acidification conditions, but net photosynthesis and growth were not affected. In contrast, rETR, net photosynthesis, and growth all decreased significantly under elevated temperature conditions (i.e. both warming and greenhouse). These results represent the imbalance of energy metabolism between electron transport and O 2 production that may be expected under ocean acidification conditions. This imbalance appears to be related to carbon and nitrogen assimilation by U. ohnoi. In particular, 13 C and 15 N discrimination data suggest U. ohnoi prefers CO 2 and NH 4 + over HCO 3 - and NO 3 - as sources of carbon and nitrogen, respectively, and this results in increased N content in the thallus under ocean acidification conditions. Together, our results suggest a trade-off in which the bloom potential of U. ohnoi could increase under ocean acidification due to greater N accumulation and through the saving of energy during carbon and nitrogen metabolism, but that elevated temperatures could decrease U. ohnoi's bloom potential through a decrease in photosynthesis and growth.

54 ENVIRONMENTAL SCIENCES↗

DOE OSTI2025

Acidification in the Southern Ocean – current state and future challenges

The Southern Ocean is especially sensitive to ocean acidification, a process where carbon dioxide in the atmosphere is absorbed by the ocean, thereby changing its acidity levels. Observations show that open ocean waters across the Southern Ocean experienced faster rates of acidification over the past four decades than non-polar waters. Model simulations project more severe ocean acidification in Antarctic coastal waters than in the open ocean. Ocean acidification negatively impacts many Southern Ocean species, but our understanding of whole-ecosystem impacts is incomplete. Furthermore, it is important that we both maintain and expand observational capabilities and mechanistic experiments in this rapidly changing and vulnerable region of the ocean to understand the impacts of ocean acidification on Southern Ocean ecosystems.

Nissen, Cara [University of Amsterdam (The Netherl↗

DOE OSTI2014

Millennial-scale ocean acidification and late Quaternary

Ocean acidification by atmospheric carbon dioxide has increased almost continuously since the last glacial maximum (LGM), 21 000 years ago. It is expected to impair tropical reef development, but effects on reefs at the present day and in the recent past have proved difficult to evaluate. We present evidence that acidification has already significantly reduced the formation of calcified bacterial crusts in tropical reefs. Unlike major reef builders such as coralline algae and corals that more closely control their calcification, bacterial calcification is very sensitive to ambient changes in carbonate chemistry. Bacterial crusts in reef cavities have declined in thickness over the past 14 000 years with largest reduction occurring 12 000 10 000 years ago. We interpret this as an early effect of deglacial ocean acidification on reef calcification and infer that similar crusts were likely to have been thicker when seawater carbonate saturation was increased during earlier glacial intervals, and thinner during interglacials. These changes in crust thickness could have substantially affected reef development over glacial cycles, as rigid crusts significantly strengthen framework and their reduction would have increased the susceptibility of reefs to biological and physical erosion. Bacterial crust decline reveals previously unrecognized millennial-scale acidification effects on tropical reefs. This directs attention to the role of crusts in reef formation and the ability of bioinduced calcification to reflect changes in seawater chemistry. It also provides a long-term context for assessing anticipated anthropogenic effects.

bacterial crust↗

DOE OSTI2014

V-ATPase-dependent luminal acidification is required for endocytic recycling of a yeast cell wall stress sensor, Wsc1p

Highlights: •A targeted genome screen identified 5 gene groups affecting Wsc1p recycling. •V-ATPase-dependent luminal acidification is required for Wsc1p recycling. •Activity of V-ATPase might be required for cargo recognition by the retromer complex. -- Abstract: Wsc1p is a major cell wall sensor protein localized at the polarized cell surface. The localization of Wsc1p is maintained by endocytosis and recycling from endosomes back to the cell surface, but changes to the vacuole when cells are subjected to heat stress. Exploiting this unique property of Wsc1p, we screened for yeast single-gene deletion mutants exhibiting defects in Wsc1p trafficking. By expressing 3GFP-tagged Wsc1p in mutants with deleted genes whose function is related to intracellular trafficking, we identified 5 gene groups affecting Wsc1p trafficking, impaired respectively in endocytic internalization, multivesicular body sorting, the GARP complex, endosomal maturation/vacuolar fusion, and V-ATPase. Interestingly, deletion of the VPH1 gene, encoding the V{sub o} subunit of vacuolar-type H{sup +}-ATPase (V-ATPase), led to mis-localization of Wsc1p from the plasma membrane to the vacuole. In addition, disruption of other V-ATPase subunits (vma mutants) also caused defects of Wsc1p trafficking and vacuolar acidification similar to those seen in the vph1Δ mutant. Moreover, we found that deletion of the VPS26 gene, encoding a subunit of the retromer complex, also caused a defect in Wsc1p recycling and mis-localization of Wsc1p to the vacuole. These findings clarified the previously unidentified Wsc1p recycling pathway and requirement of V-ATPase-dependent luminal acidification for Wsc1p recycling.

60 APPLIED LIFE SCIENCES↗

DOE OSTI2024

Water acidification aggravates lithium-induced toxicity represented by energy supply, oxidative stress, and cell fate in Daphnia magna neonates

Lithium is extensively utilized in industrial energy production, particularly in lithium-ion batteries, and in pharmaceuticals for the treating clinical mood disorders. Consequently, lithium is frequently detected in various environmental matrices. It has been reported to cause a range of toxic effects on aquatic organisms including oxidative stress, neurological disorders, and reproductive suppression. Water acidification is a global issue with numerous negative impacts on aquatic organisms. It can alter the physio-chemical properties and bioavailability of metal ions. The acidic leaching process during lithium battery treatment and global water acidification both suggest that lithium contamination often occurs in acidic environments. In the present study, Daphnia magna neonates were exposed to four treatments (control, lithium alone, low pH, and combined) to investigate whether an acidic environment exacerbates the toxic effects of lithium on aquatic organisms and to explore potential toxic action mechanisms. The results indicated that low pH posed a significant threat to the growth and reproduction of D. magna. When exposed to both lithium and low pH, there was increased lithium accumulation and an energy trade-off response, leading to increased energy allocation to reproduction and reduced energy for growth. Lithium exposure stimulated D. magna activity, while low pH inhibited it, suggesting that an imbalance in energy consumption and supply. Combined exposure to lithium and low pH resulted in severe oxidative stress due to mitochondrial dysfunction, under-utilization of energy substances, and increased ionic homeostasis disturbances. Consequently, the exposed organism altered apoptosis and autophagy processes to maintain homeostasis. In conclusion, the present study demonstrated that lithium and water acidification posed a population-level threat to D. magna, and their combined exposure significantly largely exacerbated the toxic effects.

63 RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTAN↗

DOE OSTI2012

Ocean acidification in a geoengineering context

Fundamental changes to marine chemistry are occurring because of increasing carbon dioxide (CO 2 ) in the atmosphere. Ocean acidity (H+ concentration) and bicarbonate ion concentrations are increasing, whereas carbonate ion concentrations are decreasing. There has already been an average pH decrease of 0.1 in the upper ocean, and continued unconstrained carbon emissions would further reduce average upper ocean pH by approximately 0.3 by 2100. Laboratory experiments, observations and projections indicate that such ocean acidification may have ecological and biogeochemical impacts that last for many thousands of years. The future magnitude of such effects will be very closely linked to atmospheric CO 2 ; they will, therefore, depend on the success of emission reduction, and could also be constrained by geoengineering based on most carbon dioxide removal (CDR) techniques. However, some ocean-based CDR approaches would (if deployed on a climatically significant scale) re-locate acidification from the upper ocean to the seafloor or elsewhere in the ocean interior. If solar radiation management were to be the main policy response to counteract global warming, ocean acidification would continue to be driven by increases in atmospheric CO 2 , although with additional temperature-related effects on CO 2 and CaCO 3 solubility and terrestrial carbon sequestration.

54 ENVIRONMENTAL SCIENCES↗

DOE OSTI2019

Soil Microbiome Dynamics During Pyritic Mine Tailing Phytostabilization: Understanding Microbial Bioindicators of Soil Acidification

Challenges to the reclamation of pyritic mine tailings arise from in situ acid generation that severely constrains the growth of natural revegetation. While acid mine drainage (AMD) microbial communities are well-studied under highly acidic conditions, fewer studies document the dynamics of microbial communities that generate acid from pyritic material under less acidic conditions that can allow establishment and support of plant growth. This research characterizes the taxonomic composition dynamics of microbial communities present during a 6-year compost-assisted phytostabilization field study in extremely acidic pyritic mine tailings. A complementary microcosm experiment was performed to identify successional community populations that enable the acidification process across a pH gradient. Taxonomic profiles of the microbial populations in both the field study and microcosms reveal shifts in microbial communities that play pivotal roles in facilitating acidification during the transition between moderately and highly acidic conditions. The potential co-occurrence of organoheterotrophic and lithoautotrophic energy metabolisms during acid generation suggests the importance of both groups in facilitating acidification. Taken together, this research suggests that key microbial populations associated with pH transitions could be used as bioindicators for either sustained future plant growth or for acid generation conditions that inhibit further plant growth.

37 INORGANIC, ORGANIC, PHYSICAL, AND ANALYTICAL CH↗

DOE OSTI2025

Amplified bottom water acidification rates on the Bering Sea shelf from 1970–2022

The Bering Sea shelf supports a highly productive marine ecosystem that is vulnerable to ocean acidification (OA) due to the cold, carbon-rich waters. Previous observational evidence suggests that bottom waters on the shelf are already seasonally undersaturated with respect to aragonite (i.e. Ω arag <1) and that OA will continue to increase the spatial extent, duration, and intensity of these conditions. Here, we use a regional ocean biogeochemical model to simulate changes in ocean carbon chemistry for the Bering Sea shelf from 1970–2022. Over this timeframe, model results suggest that surface Ω arag decreases by −0.043 per decade and surface pH by −0.014 per decade, comparable to observed global rates of OA. However, bottom water pH decreases at twice the rate of surface pH, while bottom [H + ] decreases at nearly 3 times the rate of surface [H + ]. This amplified bottom water acidification has emerged over the past 25 years and is likely driven by a combination of anthropogenic carbon accumulation and increasing primary productivity and subsurface respiration and remineralization. Due to this enhanced bottom water acidification, the spatial extent of bottom waters with Ω arag <1 has greatly expanded over the past 2 decades, along with pH conditions harmful to red king crab. Interannual variability in surface and bottom Ω arag , pH, and [H + ] has also increased over the past 2 decades, resulting in part from the increased physical climate variability. We also find that the Bering Sea shelf is a net annual carbon sink of 1.1–7.9 Tg C yr −1 , with the range resulting from the difference in the two different atmospheric forcing reanalysis products used. Seasonally, the shelf is a significant carbon sink from April–October but a somewhat weaker carbon source from November–March.

54 ENVIRONMENTAL SCIENCES↗

DOE OSTI2011

Hepatic steatosis inhibits autophagic proteolysis via impairment of autophagosomal acidification and cathepsin expression

Highlights: {yields} Acidification of autophagosome was blunted in steatotic hepatocytes. {yields} Hepatic steatosis did not disturb fusion of isolated autophagosome and lysosome. {yields} Proteinase activity of cathepsin B and L in autolysosomes was inhibited by steatosis. {yields} Hepatic expression of cathepsin B and L was suppressed by steatosis. -- Abstract: Autophagy, one of protein degradation system, contributes to maintain cellular homeostasis and cell defense. Recently, some evidences indicated that autophagy and lipid metabolism are interrelated. Here, we demonstrate that hepatic steatosis impairs autophagic proteolysis. Though accumulation of autophagosome is observed in hepatocytes from ob/ob mice, expression of p62 was augmented in liver from ob/ob mice more than control mice. Moreover, degradation of the long-lived protein leucine was significantly suppressed in hepatocytes isolated from ob/ob mice. More than 80% of autophagosomes were stained by LysoTracker Red (LTR) in hepatocytes from control mice; however, rate of LTR-stained autophagosomes in hepatocytes were suppressed in ob/ob mice. On the other hand, clearance of autolysosomes loaded with LTR was blunted in hepatocytes from ob/ob mice. Although fusion of isolated autophagosome and lysosome was not disturbed, proteinase activity of cathepsin B and L in autolysosomes and cathepsin B and L expression of liver were suppressed in ob/ob mice. These results indicate that lipid accumulation blunts autophagic proteolysis via impairment of autophagosomal acidification and cathepsin expression.

60 APPLIED LIFE SCIENCES↗

DOE OSTI2017

Phagolysosome acidification is required for silica and engineered nanoparticle-induced lysosome membrane permeabilization and resultant NLRP3 inflammasome activity

NLRP3 inflammasome activation occurs in response to hazardous particle exposures and is critical for the development of particle-induced lung disease. Mechanisms of Lysosome Membrane Permeabilization (LMP), a central pathway for activation of the NLRP3 inflammasome by inhaled particles, are not fully understood. We demonstrate that the lysosomal vATPases inhibitor Bafilomycin A1 blocked LMP in vitro and ex vivo in primary murine macrophages following exposure to silica, multi-walled carbon nanotubes, and titanium nanobelts. Bafilomycin A1 treatment of particle-exposed macrophages also resulted in decreased active cathepsin L in the cytosol, a surrogate measure for leaked cathepsin B, which was associated with less NLRP3 inflammasome activity. Silica-induced LMP was partially dependent upon lysosomal cathepsins B and L, whereas nanoparticle-induced LMP occurred independent of cathepsin activity. Furthermore, inhibition of lysosomal cathepsin activity with CA-074-Me decreased the release of High Mobility Group Box 1. Together, these data support the notion that lysosome acidification is a prerequisite for particle-induced LMP, and the resultant leak of lysosome cathepsins is a primary regulator of ongoing NLRP3 inflammasome activity and release of HMGB1. - Highlights: • Silica and nanoparticles cause LMP in macrophages in vitro and in vivo. • Phagolysosome acidification is required for particle-induced LMP. • Cathepsin B and L are not required for nanoparticle-induced LMP. • Cathepsin B/L regulate the secretion of HMGB1 with particle exposure.

60 APPLIED LIFE SCIENCES↗