PubMed

Related Articles Hepatic PGC-1α is not essential for fasting-induced cytochrome p450 regulation in mouse liver. Biochem Pharmacol. 2019 Nov 28;:113736 Authors: Thøgersen R, Maag Kristensen C, Algot Olsen M, Christine Bertram H, Pilegaard H, Krøyer Rasmussen M Abstract Fasting has been shown to regulate the expression of the cytochrome p450 (CYP) enzyme system in the liver. However, the exact mechanism behind the fasting-induced regulation of the CYP's remains unknown. In the present study we tested the hypothesis that the peroxisome proliferator-activated receptor gamma coactivator 1α (PGC-1α), which is a key-regulator of energy metabolism, is responsible for the fasting-induced regulation of the CYP's. Lox/lox and liver specific PGC-1α (LKO) mice of both sexes, fasted for 18 hours and the content of the CYP's as well as the hepatic metabolome was assessed. Fasting increased the mRNA content of Cyp2a4, Cyp2e1, Cyp3a11 and Cyp4a10. The fasting-induced response in Cyp4a10 mRNA content was different between lox/lox and LKO mice, while the absence of PGC-1α had no effect on the fasting-induced response for the other Cyp's. Moreover, the fasting-induced response in mRNA content of Sirtinus 1 and Perilipin 2 was different between lox/lox and LKO mice. Only the CYP1A isoform showed a fasting-induced response at the protein level. Absence of hepatic PGC-1α had no effect on the apparent metabolome, where fasting vs fed was the only discriminate in the following multivariate analysis. In conclusion, hepatic PGC-1α is not essential for the fasting-induced regulation of hepatic CYP's. PMID: 31786263 [PubMed - as supplied by publisher]

Related Articles Experimental design for parameter estimation in steady-state linear models of metabolic networks. Math Biosci. 2019 Nov 28;:108291 Authors: Frøysa HG, Skaug HJ, Alendal G Abstract Metabolic networks are typically large, containing many metabolites and reactions. Dynamical models that aim to simulate such networks will consist of a large number of ordinary differential equations, with many kinetic parameters that must be estimated from experimental data. We assume these data to be metabolomics measurements made under steady-state conditions for different input fluxes. Assuming linear kinetics, analytical criteria for parameter identifiability are provided. For normally distributed error terms, we also calculate the Fisher information matrix analytically to be used in the D-optimality criterion. A test network illustrates the developed tool chain for finding an optimal experimental design. The first stage is to verify global or pointwise parameter identifiability, the second stage to find optimal input fluxes, and finally remove redundant measurements. PMID: 31786081 [PubMed - as supplied by publisher]

Related Articles Activation of Kappa Opioid Receptor Regulates the Hypothermic Response to Calorie Restriction and Limits Body Weight Loss. Curr Biol. 2019 Nov 05;: Authors: Cintron-Colon R, Johnson CW, Montenegro-Burke JR, Guijas C, Faulhaber L, Sanchez-Alavez M, Aguirre CA, Shankar K, Singh M, Galmozzi A, Siuzdak G, Saez E, Conti B Abstract Mammals maintain a nearly constant core body temperature (Tb) by balancing heat production and heat dissipation. This comes at a high metabolic cost that is sustainable if adequate calorie intake is maintained. When nutrients are scarce or experimentally reduced such as during calorie restriction (CR), endotherms can reduce energy expenditure by lowering Tb [1-6]. This adaptive response conserves energy, limiting the loss of body weight due to low calorie intake [7-10]. Here we show that this response is regulated by the kappa opioid receptor (KOR). CR is associated with increased hypothalamic levels of the endogenous opioid Leu-enkephalin, which is derived from the KOR agonist precursor dynorphin [11]. Pharmacological inhibition of KOR, but not of the delta or the mu opioid receptor subtypes, fully blocked CR-induced hypothermia and increased weight loss during CR independent of calorie intake. Similar results were seen with DIO mice subjected to CR. In contrast, inhibiting KOR did not change Tb in animals fed ad libitum (AL). Chemogenetic inhibition of KOR neurons in the hypothalamic preoptic area reduced the CR-induced hypothermia, whereas chemogenetic activation of prodynorphin-expressing neurons in the arcuate or the parabrachial nucleus lowered Tb. These data indicate that KOR signaling is a pivotal regulator of energy homeostasis and can affect body weight during dieting by modulating Tb and energy expenditure. PMID: 31786059 [PubMed - as supplied by publisher]

Related Articles Immunosuppression by Mutated Calreticulin Released from Malignant Cells. Mol Cell. 2019 Nov 23;: Authors: Liu P, Zhao L, Loos F, Marty C, Xie W, Martins I, Lachkar S, Qu B, Waeckel-Énée E, Plo I, Vainchenker W, Perez F, Rodriguez D, López-Otin C, van Endert P, Zitvogel L, Kepp O, Kroemer G Abstract Mutations affecting exon 9 of the CALR gene lead to the generation of a C-terminally modified calreticulin (CALR) protein that lacks the KDEL endoplasmic reticulum (ER) retention signal and consequently mislocalizes outside of the ER where it activates the thrombopoietin receptor in a cell-autonomous fashion, thus driving myeloproliferative diseases. Here, we used the retention using selective hooks (RUSH) assay to monitor the trafficking of CALR. We found that exon-9-mutated CALR was released from cells in response to the biotin-mediated detachment from its ER-localized hook, in vitro and in vivo. Cellular CALR release was confirmed in suitable mouse models bearing exon-9-mutated hematopoietic systems or tumors. Extracellular CALR mediated immunomodulatory effects and inhibited the phagocytosis of dying cancer cells by dendritic cells (DC), thereby suppressing antineoplastic immune responses elicited by chemotherapeutic agents or by PD-1 blockade. Altogether, our results demonstrate paracrine immunosuppressive effects for exon-9-mutated CALR. PMID: 31785928 [PubMed - as supplied by publisher]

Related Articles High-throughput non-targeted metabolomics study of the effects of perfluorooctane sulfonate (PFOS) on the metabolic characteristics of A. thaliana leaves. Sci Total Environ. 2019 Nov 23;:135542 Authors: Guo Q, He Z, Liu X, Liu B, Zhang Y Abstract The ecotoxicity of perfluorooctane sulfonate (PFOS) is complex and has been reported in animals (including fish and mice), but the effects of PFOS in plants, especially the toxic mechanisms, have rarely been studied. High-throughput nontargeted metabolomics methods for comprehensive assessment were selected to study changes in metabolic characteristics in Arabidopsis thaliana leaves by exposure to different concentrations of PFOS throughout the growth period (30 days). All the metabolites were analyzed by PCA and OPLS-DA methods, by the cutoff of VIP and p-value, 53 biomarkers were found and significantly regulated, all amino acids except glutamate were inhibited and probably associated with binding to protein, auxin and cytokinin of phytohormones were significantly down-regulated. In response mechanism to oxidative stress from PFOS, the phenylpropanoid pathway were fully activated to form several polyphenols and further enhanced into several flavonoids against the reactive oxygen species (ROS) as the primary defend pathway, in addition, ascorbate, trehalose and nicotinamide also were activated and help decrease the damage from oxidative stress. These results provide insights into the mechanism underlying the phytotoxicity of PFOS. PMID: 31785916 [PubMed - as supplied by publisher]

Related Articles Brain and blood metabolome for Alzheimer's dementia: findings from a targeted metabolomics analysis. Neurobiol Aging. 2019 Nov 05;: Authors: Huo Z, Yu L, Yang J, Zhu Y, Bennett DA, Zhao J Abstract The development of Alzheimer's dementia (AD) accompanies both central and peripheral metabolic disturbance, but the metabolic basis underlying AD and metabolic markers predictive of AD risk remain to be determined. It is also unclear whether the metabolic changes in the peripheral blood and brain are overlapping in relation to AD. The present study addresses these questions by targeted metabolomics in both antemortem blood and postmortem brain samples in 2 community-based longitudinal cohorts of aging and dementia. We found that higher serum levels of 3 acylcarnitines, including decanoylcarnitine (C10), pimelylcarnitine (C7-DC), and tetradecadienylcarnitine (C14:2), significantly predict a lower risk of incident AD (composite hazard ratio = 0.368, 95% CI [0.207, 0.653]) after an average of 4.5-year follow-up, independent of age, sex, and education. In addition, baseline serum levels of ten glycerophospholipids, one amino acid, and 5 acylcarnitines predict the longitudinal change in cognitive functions. Moreover, 28 brain metabolites were associated with AD phenotypes. Of the putative metabolites identified in the serum and brain, 4 metabolites (3 glycerophospholipids [PC aa C30:0, PC ae C34:0, PC ae C36:1] and 1 acylcarnitine [C14:2]) were present in both the postmortem brain and antemortem blood, but only one metabolite (C14:2) was associated with AD in the same direction (i.e., protective). Partial correlation and network analyses suggest a potential tissue-specific regulation of metabolism, although other alternatives exist. Together, we identified significant associations of both central and peripheral metabolites with AD phenotypes, but there seems to be little overlap between the 2 tissues. PMID: 31785839 [PubMed - as supplied by publisher]

Related Articles Metabolic effects of repeated ketamine administration in the rat brain. Biochem Biophys Res Commun. 2019 Nov 27;: Authors: Chen F, Ye Y, Dai X, Zheng Y, Fang S, Liao L Abstract Ketamine is a popular recreational drug used in club and dance music settings. Evidence suggests that chronic or repeated ketamine use could induce neurological and psychological harm, while the mechanisms underlying ketamine's effects on the nervous system are still unclear. The aim of this study was to explore the metabolic changes that occur in the prefrontal cortex (PFC), hippocampus (Hip) and striatum of rats with repeated ketamine exposure and withdrawal intervention and to identify the potential metabolic pathways influenced by ketamine. An untargeted ultra-performance liquid chromatography-quadrupole-time-of-flight mass spectrometry (UPLC-Q-TOF-MS)-based metabolomics method coupled with multivariate and univariate statistical analysis was applied to analyze the metabolic profiles of the PFC, Hip, and striatum and to identify metabolite alterations. The pathway analysis tool in MetaboAnalyst was subsequently applied for pathway predictions. A total of 79, 54 and 58 changed metabolites were identified in the PFC, Hip and striatum, respectively, after repeated ketamine exposure. Pathway analysis indicated that purine metabolism and glycerophospholipid metabolism were the main pathways disturbed by ketamine in all three brain regions. After one week of withdrawal intervention, most changed metabolites in the Hip and striatum had been restored to control levels, while the metabolite alterations in the PFC were persistent. These results revealed that repeated ketamine exposure significantly changed purine metabolism and glycerophospholipid metabolism in the PFC, Hip and striatum, which might be involved in the neurotoxic effects of ketamine. Additionally, this study also identified that the PFC, rather than the Hip or striatum, was more likely to be the target region of the long-term effects of ketamine. PMID: 31785818 [PubMed - as supplied by publisher]

Related Articles Tween 80 induces a carbon flux rerouting in Mycobacterium tuberculosis. J Microbiol Methods. 2019 Nov 27;:105795 Authors: Pietersen RD, du Preez I, Loots DT, van Reenen M, Beukes D, Leisching G, Baker B Abstract As a means to increase the growth rate and reduce aggregation, Tween 80 is routinely added to growth media during mycobacterial culturing. This detergent has, however, been associated with causing alterations to the morphology, pathogenicity and virulence of these bacteria. In an attempt to better understand the underlying mechanism of these alterations, we investigated the effect of Tween 80 on the metabolomes of a M. tuberculosis lab strain (H37Rv) and multidrug-resistant clinical strain (R179), using GC-GCxTOF-MS metabolomics. The metabolite markers identified indicated Tween 80-induced disparities in the central carbon metabolism of both strains, with an upregulation in the glyoxylate cycle, glucogenogenesis and the pentose phosphate pathway. The results also signified an increased production of mycobacterial biosynthetic precursors such as triacylglycerols, proteinogenic amino acids and nucleotide precursors, in the presence of the detergent. Collectively, these metabolome variations mimic the phenotypic changes observed when M. tuberculosis is grown in vivo, in a lipid rich environment. However, in addition to the increased availability of oleic acid as a carbon source from Tween 80, the observed variations, and the morphological changes associated with the detergent, could also be a result of an overall stress response in these bacteria. This study is the first to identify specific metabolome variations related to the addition of Tween 80 to the growth media during M. tuberculosis culturing. The consideration of these results during the method development and data interpretation phases of future metabolomics investigations will improve the quality of the analyses as well as the credibility of potential research outcomes. These results will also assist in the interpretation of research questions specifically aimed at aspects of mycobacterial metabolism, even when using other methodologies such as transcriptomics or fluxomics. PMID: 31785333 [PubMed - as supplied by publisher]

Related Articles Study of Differential Serum Metabolites in Patients with Adenomatous Polyps of Colon and Yang-Deficiency Constitution Based on Ultra-performance Liquid Chromatography-Mass Spectrometry. Chin J Integr Med. 2019 Nov 29;: Authors: Du WZ, Zhang AH, Ren JL, Lyu K, Tuo LY, Xu W Abstract OBJECTIVE: To study the differences between the serum metabolites in patients with adenomatous polyps of the colon and yang-deficiency constitution and those without colon polyps and with balanced constitution, and look for biomarkers that can be used to distinguish between the two groups. METHODS: General patient information was gathered, and Chinese medicine constitution were collected in 940 patients who underwent electronic colonoscopy. A total of 119 patients with adenomatous polyps of the colon and yang-deficiency constitution were included in the experimental group, and 150 patients without colon polyps and with balanced constitution were included in the control group. Metabolomics analysis was performed on the fasting venous blood obtained from each patient in both groups. Principal component analysis and orthogonal partial least squares discriminant analysis were performed on the detection results, potential biomarkers were screened, metabolic pathway changes were determined, and the metabolic processes involved were discussed. RESULTS: A total of 59 differential biomarkers between the experimental group and the control group were identified. The differential metabolites were found mainly in the glycerophospholipid metabolism pathway, and the bile acid 3-oxo-4,6-choladienoic acid was the biomarker that distinguished the experimental group from the control group. CONCLUSION: With the help of metabolomics analysis, the differential metabolites in patients with adenomatous polyps of the colon and yang-deficiency constitution and those in patients without colon polyps and with balanced constitution could be identified. The biomarker 3-oxo-4,6-choladienoic acid may have potential diagnostic value in patients with adenomatous polyp of the colon and yang-deficiency constitution. (Trial Registration No. NCT02986308). PMID: 31784934 [PubMed - as supplied by publisher]

Related Articles Tryptophan metabolism is differently regulated between large and small dogs. Geroscience. 2019 Nov 29;: Authors: Hoffman JM, Kiklevich JV, Austad M, Tran V, Jones DP, Royal A, Henry C, Austad SN Abstract Companion dogs have recently been promoted as an animal model for the study of aging due to their similar disease profile to humans, the sophistication of health assessment and disease diagnosis, and the shared environments with their owners. In addition, dogs show an interesting life history trait pattern where smaller individuals are up to two-fold longer lived than their larger counterparts. While some of the mechanisms underlying this size and longevity trade-off are strongly suspected (i.e., growth hormone/IGF-I), there are likely a number of undiscovered mechanisms as well. Accordingly, we have completed a large-scale global metabolomic profiling of dogs encompassing a range of sizes and ages from three cities across the USA. We found a surprisingly strong location signal in the metabolome, stronger in fact than any signal related to age, breed, or sex. However, after controlling for the effects of location, tryptophan metabolism emerged as significantly associated with weight of the dogs, with small dogs having significantly higher levels of tryptophan pathway metabolites. Overall, our results point toward novel, testable hypotheses about the underlying physiological mechanisms that influence size and longevity in the companion dog and suggest that dogs may be useful in sorting out the complexities of the tryptophan metabolic network. PMID: 31784886 [PubMed - as supplied by publisher]

Related Articles Advances in molecular biology of Paeonia L. Planta. 2019 Nov 29;251(1):23 Authors: Fan Y, Wang Q, Dong Z, Yin Y, Teixeira da Silva JA, Yu X Abstract Molecular biology can serve as a tool to solve the limitations of traditional breeding and cultivation techniques related to flower patterns, the improvement of flower color, and the regulation of flowering and stress resistance. These characteristics of molecular biology ensured its significant role in improving the efficiency of breeding and germplasm amelioration of Paeonia. This review describes the advances in molecular biology of Paeonia, including: (1) the application of molecular markers; (2) genomics, transcriptomics, proteomics, metabolomics, and microRNA studies; (3) studies of functional genes; and (4) molecular biology techniques. This review also points out select limitations in current molecular biology, analyzes the direction of Paeonia molecular biology research, and provides advice for future research objectives. PMID: 31784828 [PubMed - in process]

Related Articles Type I Interferon Signaling Disrupts the Hepatic Urea Cycle and Alters Systemic Metabolism to Suppress T Cell Function. Immunity. 2019 Nov 22;: Authors: Lercher A, Bhattacharya A, Popa AM, Caldera M, Schlapansky MF, Baazim H, Agerer B, Gürtl B, Kosack L, Májek P, Brunner JS, Vitko D, Pinter T, Genger JW, Orlova A, Pikor N, Reil D, Ozsvár-Kozma M, Kalinke U, Ludewig B, Moriggl R, Bennett KL, Menche J, Cheng PN, Schabbauer G, Trauner M, Klavins K, Bergthaler A Abstract Infections induce complex host responses linked to antiviral defense, inflammation, and tissue damage and repair. We hypothesized that the liver, as a central metabolic hub, may orchestrate systemic metabolic changes during infection. We infected mice with chronic lymphocytic choriomeningitis virus (LCMV), performed RNA sequencing and proteomics of liver tissue, and integrated these data with serum metabolomics at different infection phases. Widespread reprogramming of liver metabolism occurred early after infection, correlating with type I interferon (IFN-I) responses. Viral infection induced metabolic alterations of the liver that depended on the interferon alpha/beta receptor (IFNAR1). Hepatocyte-intrinsic IFNAR1 repressed the transcription of metabolic genes, including Otc and Ass1, which encode urea cycle enzymes. This led to decreased arginine and increased ornithine concentrations in the circulation, resulting in suppressed virus-specific CD8+ T cell responses and ameliorated liver pathology. These findings establish IFN-I-induced modulation of hepatic metabolism and the urea cycle as an endogenous mechanism of immunoregulation. PMID: 31784108 [PubMed - as supplied by publisher]

Related Articles Auxin and cytokinin coordinate the dormancy and outgrowth of axillary bud in strawberry runner. BMC Plant Biol. 2019 Nov 29;19(1):528 Authors: Qiu Y, Guan SC, Wen C, Li P, Gao Z, Chen X Abstract BACKGROUND: Axillary buds allow the production of either vegetative or reproductive shoots, which display a plastic developmental potential of the plant to suit the prevailing environmental changes. Strawberry represents one of many plant species which displays horizontal above-ground growth of shoot development for asexual reproduction. Two distinct runner growth patterns exist in different strawberry species: one is called sympodial type such as Fragaria vesca, and the other one is called monopodial type such as Fragaria pentaphylla. Despite the runner growth morphology of these strawberry species have been well known, the mechanisms that determine the distinct patterns have rarely been reported. RESULTS: In this study, we used Fragaria vesca Hawaii-4 and Fragaria pentaphylla as model species, and captured the initiated dormant bud and non-dormant bud as materials to compare their transcriptome profiles and phytohormone content. Comparisons revealed that relatively higher auxin activity is present in the dormant bud and relatively higher cytokinin activity is in the non-dormant bud. Decapitation and pharmacological experiments on dormant buds showed that the reduction of auxin accumulation triggers the regeneration of vegetative shoots in dormant buds, and exogenous cytokinin application triggers cell fate turnover and generation of reproductive shoots. CONCLUSION: Here, we uncover a mechanism by which auxin and cytokinin coordinate the dormancy and outgrowth of axillary bud in strawberry runner. Our results suggest a contrasting behavior of auxin and cytokinin in control of axillary bud development, facilitating a preliminary understanding of shoot architecture formation in strawberry. PMID: 31783789 [PubMed - in process]

Related Articles Diet-Induced Rat Model of Gradual Development of Non-Alcoholic Fatty Liver Disease (NAFLD) with Lipopolysaccharides (LPS) Secretion. Diagnostics (Basel). 2019 Nov 27;9(4): Authors: Maciejewska D, Łukomska A, Dec K, Skonieczna-Żydecka K, Gutowska I, Skórka-Majewicz M, Styburski D, Misiakiewicz-Has K, Pilutin A, Palma J, Sieletycka K, Marlicz W, Stachowska E Abstract BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) is one of the most common liver disorders in industrialized Western countries. The prevalence of the disease is estimated to range from 4% to 46% worldwide. The aim of study was to develop an animal model with gradual NAFLD development. METHODS: Sprague-Dawley rats were fed a high-fat and high-cholesterol (HFHCh) diet. The rats from the study and control groups were sacrificed after 2, 4, 8, 12, 16, and 20 weeks of dietary exposure. RESULTS: Analysis of biochemical parameters showed that after only two weeks, ALT and cholesterol concentration in serum were elevated. After 4 weeks, TNF-α and HOMA-IR were significantly higher compared to the control group. NAFLD progression started after 12 weeks of diet-weight gain and increased LPS secretions were noticed. During the experiment, rats induced steatosis (from stage 0/1 after 4 weeks to stage 2/3 after 20 weeks), inflammation (from stage 0/1 after 4 weeks to stage 1/2 after 20 weeks), and fibrosis (from stage 1 after 12 weeks to stage 2 after 20 weeks). CONCLUSION: We can assume that the presented model based on the HFHCh diet induced gradual development of NAFLD. We confirmed that the animal NAFLD model increases LPS secretions during disease progression. PMID: 31783667 [PubMed]

Related Articles Ammonium Fluoride as Suitable Additive for HILIC-Based LC-HRMS Metabolomics. Metabolites. 2019 Nov 27;9(12): Authors: Narduzzi L, Royer AL, Bichon E, Guitton Y, Buisson C, Le Bizec B, Dervilly-Pinel G Abstract Hydrophilic Interaction Liquid Chromatography (HILIC) chromatography is widely applied in metabolomics as a complementary strategy to reverse phase chromatography. Nevertheless, it still faces several issues in terms of peak shape and compounds ionization, limiting the automatic de-convolution and data semi-quantification performed through dedicated software. A way to improve the chromatographic and ionization performance of a HILIC method is to modify the electrostatic interactions of the analytes with both mobile and stationary phases. In this study, using a ZIC-HILIC chromatographic phase, we evaluated the performance of ammonium fluoride (AF) as additive salt, comparing its performance to ammonium acetate (AA). Three comparative criteria were selected: (1) identification and peak quality of 34 standards following a metabolomics-specific evaluation approach, (2) an intraday repeatability test with real samples and (3) performing two real metabolomics fingerprints with the AF method to evaluate its inter-day repeatability. The AF method showed not only higher ionization efficiency and signal-to-noise ratio but also better repeatability and robustness than the AA approach. A tips and tricks section is then added, aiming at improving method replicability for further users. In conclusion, ammonium fluoride as additive salt presents several advantages and might be considered as a step forward in the application of robust HILIC methods in metabolomics. PMID: 31783638 [PubMed]

Related Articles Mucosal Metabolomic Profiling and Pathway Analysis Reveal the Metabolic Signature of Ulcerative Colitis. Metabolites. 2019 Nov 27;9(12): Authors: Diab J, Hansen T, Goll R, Stenlund H, Jensen E, Moritz T, Florholmen J, Forsdahl G Abstract The onset of ulcerative colitis (UC) is characterized by a dysregulated mucosal immune response triggered by several genetic and environmental factors in the context of host-microbe interaction. This complexity makes UC ideal for metabolomic studies to unravel the disease pathobiology and to improve the patient stratification strategies. This study aims to explore the mucosal metabolomic profile in UC patients, and to define the UC metabolic signature. Treatment- naïve UC patients (n = 18), UC patients in deep remission (n = 10), and healthy volunteers (n = 14) were recruited. Mucosa biopsies were collected during colonoscopies. Metabolomic analysis was performed by combined gas chromatography coupled to time-of-flight mass spectrometry (GC-TOF-MS) and ultra-high performance liquid chromatography coupled with mass spectrometry (UHPLC-MS). In total, 177 metabolites from 50 metabolic pathways were identified. The most prominent metabolome changes among the study groups were in lysophosphatidylcholine, acyl carnitine, and amino acid profiles. Several pathways were found perturbed according to the integrated pathway analysis. These pathways ranged from amino acid metabolism (such as tryptophan metabolism) to fatty acid metabolism, namely linoleic and butyrate. These metabolic changes during UC reflect the homeostatic disturbance in the gut, and highlight the importance of system biology approaches to identify key drivers of pathogenesis which prerequisite personalized medicine. PMID: 31783598 [PubMed]

Related Articles Antioxidant defenses and metabolic responses of blue mussels (Mytilus edulis) exposed to various concentrations of erythromycin. Sci Total Environ. 2020 Jan 01;698:134221 Authors: Liang R, Shao X, Shi Y, Jiang L, Han G Abstract Erythromycin, one of the most widely used macrolide antibiotics, has been detected in various aquatic environments, so erythromycin ecotoxicity should deserve more attention. In this study, blue mussels (Mytilus edulis) were exposed to erythromycin to explore its potential physiological toxicity. After 2d acute and 7d sub-acute exposure to erythromycin, blue mussel glutathione S-transferase (GST) and catalase (CAT) activities were determined with microplate methods and metabolic responses were analyzed using 1H nuclear magnetic resonance (1H NMR). The results revealed that GST was approximately 1.6 times higher in exposed mussels at 200 mg/L and higher concentrations. CAT was about 1.9 times higher in exposed mussels at 200 mg/L, indicating that erythromycin exposure led that blue mussels enhanced antioxidant responses. Low doses of erythromycin exposure had a relatively small impact on the metabolism, while high doses of erythromycin exposure (200 and 400 mg/L) disturbed metabolic balance. With the increase of erythromycin concentrations, the individual metabolic differences within the same treatment groups also increased. The significant increase in alanine, glutamate, taurine, glycine and betaine were observed after acute and subacute exposure. Betaine played an important role in protecting antioxidant enzyme activities through adjusting osmotic pressure. The metabolomic results also showed the modes of erythromycin acted on the energy metabolism, osmoregulation, nerve activities and amino acid metabolism. This study highlighted how metabolomics can provide a comprehensive picture of metabolic responses, although significant antioxidant and metabolic responses were observed at high exposure concentrations. PMID: 31783436 [PubMed - in process]

59 new pubmed citations were retrieved for your search. Click on the search hyperlink below to display the complete search results: metabolomics These pubmed results were generated on 2019/11/30PubMed comprises more than millions of citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.

17 new pubmed citations were retrieved for your search. Click on the search hyperlink below to display the complete search results: metabolomics These pubmed results were generated on 2019/11/29PubMed comprises more than millions of citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.

19 new pubmed citations were retrieved for your search. Click on the search hyperlink below to display the complete search results: metabolomics These pubmed results were generated on 2019/11/28PubMed comprises more than millions of citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.