Alumina inhibits pyrite oxidative dissolution by regulating solid film passivation layer and S, Fe, and Al speciation transformation.

The oxidation of pyrite results in the formation of a solid film passivation layer on its surface. This layer effectively hinders the direct interaction between H2O, O2, and the pyrite surface, thereby impeding the oxidation dissolution of pyrite. There are few studies on whether alumina (Al2O3), a common aluminum-containing oxide, affects the formation of a solid film passivation layer on the surface of pyrite and inhibits the oxidation dissolution of pyrite. This research investigates the impact of Al2O3 incorporation on the speciation transformation of S, Fe, and Al on the surface of pyrite during oxygen pyrite process. The oxidation of pyrite followed the "polysulfide-thiosulfate" complex oxidation pathway. When <1.5 g/L Al2O3 was introduced, it increase pyrite oxidation, whereas ≥1.5 g/L Al2O3 prevented pyrite oxidation. The process of Al2O3 dissolution results in the consumption of H+ and the subsequent release of Al3+. This, in turn, facilitates the hydrolysis of Fe3+ and Al3+ to generate a secondary mineral layer on the pyrite surface. As a result of the accumulation of S promotes the formation of polysulfide chemical (FeSn) or iron deficiency sulfide (Fe1-xS), resulting in the formation of a solid film passivation layer composed of sulfur film and secondary mineral layer. The results demonstrated that Al2O3 can promote the formation of a solid film passivation layer on the surface of pyrite, which has significant implications for controlling the oxidation dissolution process of pyrite and offers a new perspective for the source control of acid mine drainage.

Effect of copper, arsenic and nickel on pyrite-based autotrophic denitrification.

Pyritic minerals generally occur in nature together with other trace metals as impurities, that can be released during the ore oxidation. To investigate the role of such impurities, the presence of copper (Cu(II)), arsenic (As(III)) and nickel (Ni(II)) during pyrite mediated autotrophic denitrification has been explored in this study at 30 °C with a specialized microbial community of denitrifiers as inoculum. The three metal(loid)s were supplemented at an initial concentration of 2, 5, and 7.5 ppm and only Cu(II) had an inhibitory effect on the autotrophic denitrification. The presence of As(III) and Ni(II) enhanced the nitrate removal efficiency with autotrophic denitrification rates between 3.3 [7.5 ppm As(III)] and 1.6 [7.5 ppm Ni(II)] times faster than the experiment without any metal(loid) supplementation. The Cu(II) batches, instead, decreased the denitrification kinetics with 16, 40 and 28% compared to the no-metal(loid) control for the 2, 5 and 7.5 ppm incubations, respectively. The kinetic study revealed that autotrophic denitrification with pyrite as electron donor, also with Cu(II) and Ni(II) additions, fits better a zero-order model, while the As(III) incubation followed first-order kinetic. The investigation of the extracellular polymeric substances content and composition showed more abundance of proteins, fulvic and humic acids in the metal(loid) exposed biomass.

Sulphides from garlic essential oil dose-dependently change the distribution of glycerophospholipids and induce N6-tuberculosinyladenosine formation in mycobacterial cells.

The antimicrobial properties of garlic are widely known, and numerous studies confirmed its ability to inhibit the growth of Mycobacterium tuberculosis. In this work, we explored the molecular mechanism of action of sulphides present in garlic essential oil against mycobacteria. The targeted transcriptomics and untargeted LC-MS metabolomics were applied to study dose- and time-dependent metabolic changes in bacterial cells under the influence of stressing agent. Expression profiles of genes coding stress-responsive sigma factors regulatory network and metabolic observations proved that sulphides from garlic essential oil are an efficient and specific agent affecting glycerophospholipids levels and their distribution within the cell envelope. Additionally, sulphides induced the Dimroth rearrangement of 1-Tuberculosinyladenosine to N6-tuberculosinyladenosine in mycobacterial cells as a possible neutralization mechanism protecting the cell from a basic nucleophilic environment. Sulphides affected cell envelope lipids and formation of N6-tuberculosinyladenosine in M. tuberculosis.

Dissimilatory sulfate reduction in an anaerobic biofilm reactor for tofu processing wastewater treatment: Bacterial community and their functional genes.

Dissimilatory sulfate reduction (DSR) is the key sulfur cycle that transforms sulfate to sulfide. This process leads to odour issues in wastewater treatment. However, few studies have focused on DSR during treating food processing wastewater with high sulfate. This study investigated DSR microbial population and functional genes in an anaerobic biofilm reactor (ABR) treating tofu processing wastewater. The tofu processing wastewater is a common food processing wastewater in Asia. The full-scale ABR was operated for over 120 days in a tofu and tofu-related products manufacturing factory. Mass balance calculations based on the reactor performance indicated that 79.6-85.1 % of the sulfate was transformed into sulfide irrelevant to dissolved oxygen supplementation. Metagenomic analysis revealed 21 metagenome-assembled genomes (MAGs) containing enzymes encoding DSR. The biofilm contained the complete functional genes of DSR pathway in the full-scale ABR, indicating that biofilm could process DSR independently. Comamonadaceae, Thiobacillus, Nitrosomonadales, Desulfatirhabdium butyrativorans, Desulfomonile tiedjei were the dominant DSR species in the ABR biofilm community. Dissolved oxygen supplementation directly inhibited DSR and mitigated HS- production. It was also found that Thiobacillus contained all the function genes encoding every necessary enzyme in DSR, and thus Thiobacillus distribution directly correlated to DSR and the ABR performance.

Effects of duration of exposure, co-supplementation with iron and Nippostrongylus brasiliensis infection on accumulation of trichloroacetic acid-insoluble copper in rats given molybdate in drinking water.

Thiolation can convert molybdate (MoO4) into a series of thiomolybdates (MoSxO4-x) in the rumen, terminating in tetrathiomolybdate (MoS4), a potent antagonist of copper absorption and, if absorbed, donor of reactive sulphide in tissues. Systemic exposure to MoS4 increases trichloroacetic acid-insoluble copper (TCAI Cu) concentrations in the plasma of ruminants and induction of TCAI Cu in rats given MoO4 in drinking water would support the hypothesis that rats, like ruminants, can thiolate MoO4. Data on TCAI Cu are presented from two experiments involving MoO4 supplementation that had broader objectives. In experiment 1, plasma Cu concentrations (P Cu) tripled in female rats infected with Nippostrongylus brasiliensis after only 5 days exposure to drinking water containing 70 mg Mo L-1, due largely to an increase in TCAI Cu; activities of erythrocyte superoxide dismutase and plasma caeruloplasmin oxidase (CpOA) were unaffected. Exposure for 45-51 days did not raise P Cu further but TCA-soluble (TCAS) Cu concentrations increased temporarily 5 days post infection (dpi) and weakened the linear relationship between CpOA and TCAS Cu. In experiment 2, infected rats were given less MoO4 (10 mg Mo L-1), with or without iron (Fe, 300 mg L-1), for 67 days and killed 7 or 9 dpi. P Cu was again tripled by MoO4 but co-supplementation with Fe reduced TCAI Cu from 65 ± 8.9 to 36 ± 3.8 µmol L-l. Alone, Fe and MoO4 each reduced TCAS Cu in females and males when values were higher (7 and 9 dpi, respectively). Thiolation probably occurred in the large intestine but was inhibited by precipitation of sulphide as ferrous sulphide. Fe alone may have inhibited caeruloplasmin synthesis during the acute phase response to infection, which impacts thiomolybdate metabolism.

Sulfur, sterol and trehalose metabolism in the deep-sea hydrocarbon seep tubeworm Lamellibrachia luymesi.

BACKGROUND: Lamellibrachia luymesi dominates cold sulfide-hydrocarbon seeps and is known for its ability to consume bacteria for energy. The symbiotic relationship between tubeworms and bacteria with particular adaptations to chemosynthetic environments has received attention. However, metabolic studies have primarily focused on the mechanisms and pathways of the bacterial symbionts, while studies on the animal hosts are limited. RESULTS: Here, we sequenced the transcriptome of L. luymesi and generated a transcriptomic database containing 79,464 transcript sequences. Based on GO and KEGG annotations, we identified transcripts related to sulfur metabolism, sterol biosynthesis, trehalose synthesis, and hydrolysis. Our in-depth analysis identified sulfation pathways in L. luymesi, and sulfate activation might be an important detoxification pathway for promoting sulfur cycling, reducing byproducts of sulfide metabolism, and converting sulfur compounds to sulfur-containing organics, which are essential for symbiotic survival. Moreover, sulfide can serve directly as a sulfur source for cysteine synthesis in L. luymesi. The existence of two pathways for cysteine synthesis might ensure its participation in the formation of proteins, heavy metal detoxification, and the sulfide-binding function of haemoglobin. Furthermore, our data suggested that cold-seep tubeworm is capable of de novo sterol biosynthesis, as well as incorporation and transformation of cycloartenol and lanosterol into unconventional sterols, and the critical enzyme involved in this process might have properties similar to those in the enzymes from plants or fungi. Finally, trehalose synthesis in L. luymesi occurs via the trehalose-6-phosphate synthase (TPS) and trehalose-6-phosphate phosphatase (TPP) pathways. The TPP gene has not been identified, whereas the TPS gene encodes a protein harbouring conserved TPS/OtsA and TPP/OtsB domains. The presence of multiple trehalases that catalyse trehalose hydrolysis could indicate the different roles of trehalase in cold-seep tubeworms. CONCLUSIONS: We elucidated several molecular pathways of sulfate activation, cysteine and cholesterol synthesis, and trehalose metabolism. Contrary to the previous analysis, two pathways for cysteine synthesis and the cycloartenol-C-24-methyltransferase gene were identified in animals for the first time. The present study provides new insights into particular adaptations to chemosynthetic environments in L. luymesi and can serve as the basis for future molecular studies on host-symbiont interactions and biological evolution.

Sulfide inhibition on polyphosphate accumulating organisms and glycogen accumulating organisms: Cumulative inhibitory effect and recoverability.

Sulfate in wastewater can be reduced to sulfide and its impact on the stability of enhanced biological phosphorus removal (EBPR) is still unclear. In this study, the metabolic changes and subsequent recovery of polyphosphate accumulating organisms (PAOs) and glycogen accumulating organisms (GAOs) were investigated at different sulfide concentrations. The results showed that the metabolic activity of PAOs and GAOs was mainly related to H2S concentration. Under anaerobic conditions, the catabolism of PAOs and GAOs was promoted at H2S concentrations below 79 mg/L S and 271 mg/L S, respectively, and inhibited above these concentrations; whereas anabolism was consistently inhibited in the presence of H2S. The phosphorus (P) release was also pH-dependent due to the intracellular free Mg2+ efflux from PAOs. H2S was more destructive to the esterase activity and membrane permeability of PAOs than those of GAOs and prompted intracellular free Mg2+ efflux of PAOs, resulting in worse aerobic metabolism and subsequent recovery of PAOs than GAOs. Additionally, sulfides facilitated the production of extracellular polymeric substances (EPS), especially tightly bound EPS. The amount of EPS in GAOs was significantly higher than that in PAOs. The above results indicated that sulfide had a stronger inhibition to PAOs than GAOs, and when sulfide was present, GAOs had a competitive advantage over PAOs in EBPR.

Contribution of NRF2 to sulfur metabolism and mitochondrial activity.

NF-E2-related factor 2 (NRF2) plays a crucial role in the maintenance of cellular homeostasis by regulating various enzymes and proteins that are involved in the redox reactions utilizing sulfur. While substantial impacts of NRF2 on mitochondrial activity have been described, the precise mechanism by which NRF2 regulates mitochondrial function is still not fully understood. Here, we demonstrated that NRF2 increased intracellular persulfides by upregulating the cystine transporter xCT encoded by Slc7a11, a well-known NRF2 target gene. Persulfides have been shown to play an important role in mitochondrial function. Supplementation with glutathione trisulfide (GSSSG), which is a form of persulfide, elevated the mitochondrial membrane potential (MMP), increased the oxygen consumption rate (OCR) and promoted ATP production. Persulfide-mediated mitochondrial activation was shown to require the mitochondrial sulfur oxidation pathway, especially sulfide quinone oxidoreductase (SQOR). Consistently, NRF2-mediated mitochondrial activation was also dependent on SQOR activity. This study clarified that the facilitation of persulfide production and sulfur metabolism in mitochondria by increasing cysteine availability is one of the mechanisms for NRF2-dependent mitochondrial activation.

SOD1 is an essential H2S detoxifying enzyme.

Although hydrogen sulfide (H2S) is an endogenous signaling molecule with antioxidant properties, it is also cytotoxic by potently inhibiting cytochrome c oxidase and mitochondrial respiration. Paradoxically, the primary route of H2S detoxification is thought to occur inside the mitochondrial matrix via a series of relatively slow enzymatic reactions that are unlikely to compete with its rapid inhibition of cytochrome c oxidase. Therefore, alternative or complementary cellular mechanisms of H2S detoxification are predicted to exist. Here, superoxide dismutase [Cu-Zn] (SOD1) is shown to be an efficient H2S oxidase that has an essential role in limiting cytotoxicity from endogenous and exogenous sulfide. Decreased SOD1 expression resulted in increased sensitivity to H2S toxicity in yeast and human cells, while increased SOD1 expression enhanced tolerance to H2S. SOD1 rapidly converted H2S to sulfate under conditions of limiting sulfide; however, when sulfide was in molar excess, SOD1 catalyzed the formation of per- and polysulfides, which induce cellular thiol oxidation. Furthermore, in SOD1-deficient cells, elevated levels of reactive oxygen species catalyzed sulfide oxidation to per- and polysulfides. These data reveal that a fundamental function of SOD1 is to regulate H2S and related reactive sulfur species.

Sand supplementation favors tropical seagrass Thalassia hemprichii in eutrophic bay: implications for seagrass restoration and management.

BACKGROUND: Sediment is crucial for the unique marine angiosperm seagrass growth and successful restoration. Sediment modification induced by eutrophication also exacerbates seagrass decline and reduces plantation and transplantation survival rates. However, we lack information regarding the influence of sediment on seagrass photosynthesis and the metabolics, especially regarding the key secondary metabolic flavone. Meanwhile, sulfation of flavonoids in seagrass may mitigate sulfide intrusion, but limited evidence is available. RESULTS: We cultured the seagrass Thalassia hemprichii under controlled laboratory conditions in three sediment types by combining different ratios of in-situ eutrophic sediment and coarse beach sand. We examined the effects of beach sand mixed with natural eutrophic sediments on seagrass using photobiology, metabolomics and isotope labelling approaches. Seagrasses grown in eutrophic sediments mixed with beach sand exhibited significantly higher photosynthetic activity, with a larger relative maximum electron transport rate and minimum saturating irradiance. Simultaneously, considerably greater belowground amino acid and flavonoid concentrations were observed to counteract anoxic stress in eutrophic sediments without mixed beach sand. This led to more positive belowground stable sulfur isotope ratios in eutrophic sediments with a lower Eh. CONCLUSIONS: These results indicated that coarse beach sand indirectly enhanced photosynthesis in T. hemprichii by reducing sulfide intrusion with lower amino acid and flavonoid concentrations. This could explain why T. hemprichii often grows better on coarse sand substrates. Therefore, it is imperative to consider adding beach sand to sediments to improve the environmental conditions for seagrass and restore seagrass in eutrophic ecosystems.

Understanding the Activation of Platelets in Diabetes and Its Modulation by Allyl Methyl Sulfide, an Active Metabolite of Garlic.

BACKGROUND: Diabetes mellitus (DM) is a chronic metabolic disorder associated with higher risk of having cardiovascular disease. Platelets play a promising role in the pathogenesis of cardiovascular complications in diabetes. Since last several decades, garlic and its bioactive components are extensively studied in diabetes and its complications. Our aim was to explore the antiplatelet property of allyl methyl sulfide (AMS) focusing on ameliorating platelet activation in diabetes. METHOD: We used streptozotocin- (STZ-) induced diabetic rats as model for type 1 diabetes. We have evaluated the effect of allyl methyl sulfide on platelet activation by administrating AMS to diabetic rats for 10 weeks. Flow cytometry-based analysis was used to evaluate the platelet activation, platelet aggregation, platelet macrophage interaction, and endogenous ROS generation in the platelets obtained from control, diabetes, and AMS- and aspirin-treated diabetic rats. RESULTS: AMS treatment for 10 weeks effectively reduced the blood glucose levels in diabetic rats. Three weeks of AMS (50 mg/kg/day) treatment did not reduce the activation of platelets but a significant (p < 0.05) decrease was observed after 10 weeks of treatment. Oral administration of AMS significantly (p < 0.05) reduced the baseline and also reduced ADP-induced aggregation of platelets after 3 and 10 weeks of treatment. Furthermore, 10 weeks of AMS treatment in diabetic rats attenuated the endogenous ROS content (p < 0.05) of platelets and platelet macrophage interactions. The inhibition of platelet activation in diabetic rats after AMS treatment was comparable with aspirin treatment (30 mg/kg/day). CONCLUSION: We observed an inhibitory effect of allyl methyl sulfide on platelet aggregation, platelet activation, platelet macrophage interaction, and increased ROS levels in type 1 diabetes. Our data suggests that AMS can be useful to control cardiovascular complication in diabetes via inhibition of platelet activation.

Formation of cadmium sulfide nanoparticles mediates cadmium resistance and light utilization of the deep-sea bacterium Idiomarina sp. OT37-5b.

Heavy metal is one of the major factors threatening the survival of microorganisms. Here, a deep-sea bacterium designated Idiomarina sp. OT37-5b possessing strong cadmium (Cd) tolerance was isolated from a typical hydrothermal vent. Both the Cd-resistance and removal efficiency of Idiomarina sp. OT37-5b were significantly promoted by the supplement of cysteine and meanwhile large amount of CdS nanoparticles were observed. Production of H2 S from cysteine catalysed by methionine gamma-lyase was further demonstrated to contribute to the formation of CdS nanoparticles. Proteomic results showed the addition of cysteine effectively enhanced the efflux of Cd, improved the activities of reactive oxygen species scavenging enzymes, and thereby boosted the nitrogen reduction and energy production of Idiomarina sp. OT37-5b. Notably, the existence of CdS nanoparticles obviously promoted the growth of Idiomarina sp. OT37-5b when exposed to light, indicating this bacterium might grab light energy through CdS nanoparticles. Proteomic analysis revealed the expression levels of essential components for light utilization including electron transport, cytochrome complex and F-type ATPase were significantly up-regulated, which strongly suggested the formation of CdS nanoparticles promoted light utilization and energy production. Our results provide a good model to investigate the uncovered mechanisms of self-photosensitization of nonphotosynthetic bacteria for light-to-chemical production in the deep biosphere.

Botanical sulfane sulfur donors inhibit ferroptotic cell death caused by the depletion of cysteine.

Inhibitors against cystine-glutamate antiporter, including erastin, elicit ferroptotic cell death. The erastin-induced ferroptotic cell death appears to be caused by cysteine as well as glutathione depletion. Cysteine is an essential substrate for sulfane sulfur producing systems in cells, generating persulfides that function as intracellular antioxidants and intermediates in iron-sulfur cluster production. Therefore, we examined whether botanical sulfane sulfur donors such as diallyl trisulfide (DATS) and dimethyl trisulfide (DMTS) prevent ferroptotic cell death in HT1080 cells treated with erastin. As a result, DMTS (20 µM) and DATS (10 µM) rescued the erastin-treated HT1080 cells by 69.6% and 91.6%, respectively. Furthermore, DMTS-containing squeeze of cabbage (2.0 g/L) and DATS-containing squeeze of garlic (0.07 g/L) rescued the erastin-treated HT1080 cells by 76.5% and almost 100%, respectively. In conclusion, the ingestion of trisulfides may bring about increased resistance to ferroptotic cell death in vivo.

Coenzyme Q10 modulates sulfide metabolism and links the mitochondrial respiratory chain to pathways associated to one carbon metabolism.

Abnormalities of one carbon, glutathione and sulfide metabolisms have recently emerged as novel pathomechanisms in diseases with mitochondrial dysfunction. However, the mechanisms underlying these abnormalities are not clear. Also, we recently showed that sulfide oxidation is impaired in Coenzyme Q10 (CoQ10) deficiency. This finding leads us to hypothesize that the therapeutic effects of CoQ10, frequently administered to patients with primary or secondary mitochondrial dysfunction, might be due to its function as cofactor for sulfide:quinone oxidoreductase (SQOR), the first enzyme in the sulfide oxidation pathway. Here, using biased and unbiased approaches, we show that supraphysiological levels of CoQ10 induces an increase in the expression of SQOR in skin fibroblasts from control subjects and patients with mutations in Complex I subunits genes or CoQ biosynthetic genes. This increase of SQOR induces the downregulation of the cystathionine ß-synthase and cystathionine γ-lyase, two enzymes of the transsulfuration pathway, the subsequent downregulation of serine biosynthesis and the adaptation of other sulfide linked pathways, such as folate cycle, nucleotides metabolism and glutathione system. These metabolic changes are independent of the presence of sulfur aminoacids, are confirmed in mouse models, and are recapitulated by overexpression of SQOR, further proving that the metabolic effects of CoQ10 supplementation are mediated by the overexpression of SQOR. Our results contribute to a better understanding of how sulfide metabolism is integrated in one carbon metabolism and may explain some of the benefits of CoQ10 supplementation observed in mitochondrial diseases.

Allylmethylsulfide, a Sulfur Compound Derived from Garlic, Attenuates Isoproterenol-Induced Cardiac Hypertrophy in Rats.

Allylmethylsulfide (AMS) is a novel sulfur metabolite found in the garlic-fed serum of humans and animals. In the present study, we have observed that AMS is safe on chronic administration and has a potential antihypertrophic effect. Chronic administration of AMS for 30 days did not cause any significant differences in the body weight, electrocardiogram, food intake, serum biochemical parameters, and histopathology of vital organs. Single-dose pharmacokinetics of AMS suggests that AMS is rapidly metabolized into Allylmethylsulfoxide (AMSO) and Allylmethylsulfone (AMSO2). To evaluate the efficacy of AMS, cardiac hypertrophy was induced by subcutaneous implantation of ALZET® osmotic minipump containing isoproterenol (~5 mg/kg/day), cotreated with AMS (25 and 50 mg/kg/day) and enalapril (10 mg/kg/day) for 2 weeks. AMS and enalapril significantly reduced cardiac hypertrophy as studied by the heart weight to body weight ratio and mRNA expression of fetal genes (ANP and ß-MHC). We have observed that TBARS, a parameter of lipid peroxidation, was reduced and the antioxidant enzymes (glutathione, catalase, and superoxide dismutase) were improved in the AMS and enalapril-cotreated hypertrophic hearts. The extracellular matrix (ECM) components such as matrix metalloproteinases (MMP2 and MMP9) were significantly upregulated in the diseased hearts; however, with the AMS and enalapril, it was preserved. Similarly, caspases 3, 7, and 9 were upregulated in hypertrophic hearts, and with the AMS and enalapril treatment, they were reduced. Further to corroborate this finding with in vitro data, we have checked the nuclear expression of caspase 3/7 in the H9c2 cells treated with isoproterenol and observed that AMS cotreatment reduced it significantly. Histopathological investigation of myocardium suggests AMS and enalapril treatment reduced fibrosis in hypertrophied hearts. Based on our experimental results, we conclude that AMS, an active metabolite of garlic, could reduce isoproterenol-induced cardiac hypertrophy by reducing oxidative stress, apoptosis, and stabilizing ECM components.

Control of protein function through oxidation and reduction of persulfidated states.

Irreversible oxidation of Cys residues to sulfinic/sulfonic forms typically impairs protein function. We found that persulfidation (CysSSH) protects Cys from irreversible oxidative loss of function by the formation of CysSSO1-3H derivatives that can subsequently be reduced back to native thiols. Reductive reactivation of oxidized persulfides by the thioredoxin system was demonstrated in albumin, Prx2, and PTP1B. In cells, this mechanism protects and regulates key proteins of signaling pathways, including Prx2, PTEN, PTP1B, HSP90, and KEAP1. Using quantitative mass spectrometry, we show that (i) CysSSH and CysSSO3H species are abundant in mouse liver and enzymatically regulated by the glutathione and thioredoxin systems and (ii) deletion of the thioredoxin-related protein TRP14 in mice altered CysSSH levels on a subset of proteins, predicting a role for TRP14 in persulfide signaling. Furthermore, selenium supplementation, polysulfide treatment, or knockdown of TRP14 mediated cellular responses to EGF, suggesting a role for TrxR1/TRP14-regulated oxidative persulfidation in growth factor responsiveness.

Boiling down the cysteine-stabilized LTP fold - loss of structural and immunological integrity of allergenic Art v 3 and Pru p 3 as a consequence of irreversible lanthionine formation.

BACKGROUND: Non-specific lipid transfer proteins (LTPs) are important allergens in fruits, pollen, vegetables, nuts and latex. Due to their compact structure, LTPs are highly resistant to heat treatment. Here, Art v 3 from mugwort pollen and Pru p 3 from peach were used as model allergens to in-depth investigate structural and immunological properties upon thermal treatment at different buffer conditions. METHODS: Recombinant Art v 3 and Pru p 3 were purified from E. coli and incubated at 95 °C up to 120 min using sodium phosphate buffer pH 3.4 or 7.3. Physicochemical properties of allergens were analyzed in circular dichroism spectroscopy, Fourier transform infrared spectroscopy, dynamic light scattering, size exclusion chromatography, and mass spectrometry. The crystal structure of Art v 3.0201 was determined to 1.9 Šresolution. IgG and IgE binding was investigated in ELISA using murine and LTP allergic patients' sera. RESULTS: Highly pure and homogenous recombinant allergens were obtained from bacterial production. The crystal structure of Art v 3.0201 revealed an antiparallel four helix bundle with a C-terminal extension mediating an asymmetric, transient dimer interface and differently sized cavities. Both allergens showed high thermal stability at acidic conditions. In contrast, extensive heat treatment in neutral buffer induced irreversible structural changes due to lanthionine-based cysteine rearrangement. This fostered loss of the typical α-helical structure, increased molecular size and abrogation of IgG and IgE binding epitopes. Pru p 3 lost its structural integrity at shorter heat stress duration than Art v 3, which did however only partially affect the molecule's IgE binding epitopes. CONCLUSION: During thermal treatment, susceptibility to structural changes of the LTP-fold is highly dependent on the surrounding environment but also on intrinsic features of individual LTPs. This is a crucial fact to consider when processing LTP-containing food or food products as this will directly influence their allergenic potential.

Platelet-membrane-camouflaged bismuth sulfide nanorods for synergistic radio-photothermal therapy against cancer.

Bismuth-containing nanoparticles (BNPs) are potential enhancers for tumor radiotherapy. Improving the bioavailability and developing synergistic therapeutic regimens benefit the drug transformation of BNPs. In the present study, we prepare a mesoporous silica-coated bismuth nanorod (BMSNR) camouflaged by a platelet membrane (PM). This biomimetic material is termed BMSNR@PM. The PM camouflage enhances the immune escape of the BMSNRs by lowering endocytosis by macrophages in the reticuloendothelial system. Additionally, the PM camouflage strengthens the material tumor-targeting capacity and leads to better radiotherapeutic efficacy compared with bare BMSNRs. Owing to the photothermal effect, BMSNR@PMs alters the cell cycle of 4T1 cancer cells post-treatment with 808 nm near-infrared irradiation (NIR). The proportions of S phase and G2/M phase cells decrease and increase, respectively, which explains the synergistic effect of NIR on BMSNR@PM-based radiotherapy. BMSNR@PMs efficiently eradicates cancer cells by the combined action of photothermal therapy (PTT) and radiotherapy in vivo and markedly improves the survival of 4T1-tumor-bearing mice. The synergistic therapeutic effect is superior to the outcomes of PTT and radiotherapy performed alone. Our study demonstrates a versatile bismuth-containing nanoplatform with tumor-targeting, immune escape, and radiosensitizing functionalities using an autologous cell membrane biomimetic concept that may promote the development of radiotherapy enhancers.

Quantification of volatile metabolites derived from garlic in human breast milk.

Maternal garlic intake during pregnancy and the breastfeeding period has been reported to be associated with the potential of modulating later garlic acceptance in infants. However, the metabolism of garlic constituents in humans and their elimination and potential excretion into human milk are not yet fully understood. In previous studies, we identified volatile garlic-derived metabolites in human milk as well as in human urine, namely allyl methyl sulfide, allyl methyl sulfoxide and allyl methyl sulfone. To monitor the excretion of these garlic metabolites in a larger cohort, we quantified these metabolites in a total of 18 human milk sets, whereby each set comprised of one sample collected before and three samples after garlic consumption. The analyses revealed that the concentrations of the metabolites were most abundant 1-3.5 h after garlic consumption, with distinct differences between test persons regarding metabolite concentrations as well as temporal excretion.

Bacterial interactions during sequential degradation of cyanobacterial necromass in a sulfidic arctic marine sediment.

Seafloor microorganisms impact global carbon cycling by mineralizing vast quantities of organic matter (OM) from pelagic primary production, which is predicted to increase in the Arctic because of diminishing sea ice cover. We studied microbial interspecies-carbon-flow during anaerobic OM degradation in arctic marine sediment using stable isotope probing. We supplemented sediment incubations with 13 C-labeled cyanobacterial necromass (spirulina), mimicking fresh OM input, or acetate, an important OM degradation intermediate and monitored sulfate reduction rates and concentrations of volatile fatty acids (VFAs) during substrate degradation. Sequential 16S rRNA gene and transcript amplicon sequencing and fluorescence in situ hybridization combined with Raman microspectroscopy revealed that only few bacterial species were the main degraders of 13 C-spirulina necromass. Psychrilyobacter, Psychromonas, Marinifilum, Colwellia, Marinilabiaceae and Clostridiales species were likely involved in the primary hydrolysis and fermentation of spirulina. VFAs, mainly acetate, produced from spirulina degradation were mineralized by sulfate-reducing bacteria and an Arcobacter species. Cellular activity of Desulfobacteraceae and Desulfobulbaceae species during acetoclastic sulfate reduction was largely decoupled from relative 16S rRNA gene abundance shifts. Our findings provide new insights into the identities and physiological constraints that determine the population dynamics of key microorganisms during complex OM degradation in arctic marine sediments.© 2018 Society for Applied Microbiology and John Wiley & Sons Ltd.