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This research was supported by grants from CNPq ELS , FAPESC ELS , and UNESC ELS. ELS is a 1D CNPq Research Fellow. Laboratório de Bioenergética, Programa de Pós-Graduação em Ciências da Saúde, Universidade do Extremo Sul Catarinense, Av.

Universitária, , Criciúma, SC, , Brazil. Brena P. Teodorak, Giselli Scaini, Milena Carvalho-Silva, Lara M. Gomes, Letícia J. Teixeira, Joyce Rebelo, Samira D. Instituto Nacional de Ciência e Tecnologia Translacional em Medicina INCT-TM , Porto Alegre, RS, Brazil. Núcleo de Excelência em Neurociências Aplicadas de Santa Catarina NENASC , Florianópolis, Santa Catarina, Brazil.

Laboratório de Erros Inatos do Metabolismo, Programa de Pós-Graduação em Ciências da Saúde, Universidade do Extremo Sul Catarinense, Criciúma, SC, Brazil. Laboratório de Neuroquímica, Instituto de Bioquímica Médica, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.

You can also search for this author in PubMed Google Scholar. Correspondence to Emilio L. Reprints and permissions. Teodorak, B. et al. Antioxidants reverse the changes in energy metabolism of rat brain after chronic administration of L. Metab Brain Dis 32 , — For maximum benefits, take as directed every day.

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Ocean acidification decreases mussel byssal attachment strength and induces molecular byssal responses. Ocean acidification adversely influences metabolism, extracellular pH and calcification of an economically important marine bivalve. Tegillarca granosa. Keywords : ocean acidification, energy metabolism, oxidative stress, physiological response, scallop.

Citation: Liao H, Yang Z, Dou Z, Sun F, Kou S, Zhang Z, Huang X and Bao Z Impact of Ocean Acidification on the Energy Metabolism and Antioxidant Responses of the Yesso Scallop Patinopecten yessoensis. Received: 02 September ; Accepted: 31 December ; Published: 21 January Copyright © Liao, Yang, Dou, Sun, Kou, Zhang, Huang and Bao.

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Mitochondrial abnormalities including alterations in energy metabolism have been implicated in the pathobiology of affective disorders 43 , 44 , We propose that ketamine treatment causes a cellular energy deficit by first promoting anabolic processes that consume ATP through the activation of mTORC1.

This is counterbalanced in a second phase by the activation of AMPK that promotes catabolic pathways to generate ATP. Ketamine affects glutamate neurotransmission and is tightly linked to mitochondrial energy metabolism.

Upon release, glutamate is taken up by glial cells and subsequently metabolized to glutamine. In addition, other studies have shown elevated medial prefrontal cortex metabolism and an involvement of mitochondria in MDD pathobiology 43 , 47 , 48 , Mitochondrial respiration in peripheral blood mononuclear cells from depressed patients is lower compared to cells from control subjects and correlates with depressive symptom severity Furthermore, mitochondrial disorders are often comorbid with psychiatric disorders including MDD and patients frequently suffer from TRD.

These patients have a primary impairment of mitochondrial functioning through either nuclear or mitochondrial DNA mutations. Mitochondrial impairment mostly affects high energy consuming organs like muscles and brain.

The mitochondrial disorder is often recognized only later in life of MDD patients 51 , 52 , Previous studies have connected the antidepressant response with drugs elevating ATP levels.

Spectroscopy data have shown decreased NPT levels mainly ATP in the brain of depressed patients. Another magnetic resonance spectroscopy study could demonstrate lower NPT levels mainly ATP in fluoxetine responders compared with non-responders. Previous data from a study in rats have suggested that the antidepressant-like effect observed after a single injection of ketamine is mediated by an increased anabolic rate-mediating cell growth and differentiation, processes that are highly energy consuming 54 , We submit that mitochondria play a critical role in the development of MDD as well as AD treatment response, at least in a subset of patients with a defined symptomatology.

We identified several pathways that were affected and associated with mitochondrial energy metabolism. The PLS-DA showed a time-dependent separation of ketamine- and vehicle-treated mice that was evident by significant protein level alterations and overrepresented pathways.

Ketamine affects the OXPHOS pathway as is evident by several complex I protein levels Ndufv2, Cyc1, Ndufaf7 and TmemB that correlate with FST floating time in a treatment time-dependent manner. Taken together, we propose a mechanism by which ketamine stimulates glutamatergic neurotransmission and neuronal activity, ultimately resulting in a long-term potentiation LTP -like process.

This activation results in the activation of mTORC1. Furthermore, other studies indicated that mTOR inhibition decreases mitochondrial respiration, whereas mTOR hyperactivation elevates the expression of oxidative metabolism genes and mitochondrial DNA copy number 56 , 57 , Hence, ketamine may not only increase protein translation through mTORC1, but also mitochondrial biogenesis.

LTP-like processes require energy in the form of ATP followed by AMPK activation, which we found in the present study, in order to promote catabolic processes to generate ATP. This long-term effect can be explained by the observed LTP-like process.

Late phase LTP with spine formation and strengthening of synaptic connections are known to last from days to weeks. Increased OXPHOS activity can result in elevated ROS levels, a phenomenon referred to as oxidative stress, which causes protein, DNA, RNA and lipid modifications and damage.

This can be explained by either decreased ROS levels or alternatively by an activation of a cellular defense system that captures ROS. The cellular defense system includes antioxidant molecules and enzymes such as Prdxs that combat ROS. In addition, a protein quality control system that degrades damaged proteins counteracts oxidative stress 38 , 39 , 40 , 41 , 59 , vehicle-treated mice.

The reduced protein carbonylation we observed in ketamine- vs. vehicle-treated mice could be indicative of increased protein quality control processes in the cell. Taken together, our combined proteomic results suggest that ketamine administration in mice leads to increased degradation of damaged proteins and homeostatic redox adjustment.

The close connection between the glutamatergic system and mitochondrial energy metabolism make a compelling case for the here observed facilitative effects of energy metabolism and the antioxidant defense system following ketamine administration.

Further experiments including blocking pathway enzymes and receptors including OXPHOS complex I and AMPK that we found to be involved as well as different ketamine doses are required to confirm these findings.

The animals and ketamine treatment were housed and carried out as previously described The protocols were approved by the committee for the Care and Use of Laboratory Animals of the Government of Upper Bavaria, Germany.

The forced swim test and floating time analysis were carried out as previously described CF and MF were prepared by repeated tissue homogenization and extraction of non-MF proteins and solubilization of MF proteins with sodium dodecyl sulfate SDS.

Pellets were rehomogenized in 0. After electrophoresis, proteins were transferred to PVDF membranes Immobilon-P, Millipore, Billerica, USA. Primary antibodies were against adenosinmonophosphate-activated protein kinase AMPK, Abcam, Cambridge, UK , phosphorylated AMPK pAMPK, Cell Signaling, Merck, Darmstadt, Germany , peroxiredoxin 1 Prdx1, Abcam, Cambridge, UK , peroxiredoxin 3 Prdx3, Abcam, Cambridge, UK.

Anti-rabbit, anti-mouse and anti-goat ECL horseradish peroxidase-linked secondary antibodies GE Healthcare Life Sciences, Little Chalfont, Buckinghamshire, UK were used. The densitometric analyses were performed with the Image Lab software Bio-Rad, Munich, Germany.

Hippocampal CF and MF proteins were mixed with CF and MF 15 N-labeled protein standards, respectively. Each gel lane was cut into 16 2. The supernatant was discarded and this step repeated twice.

Hippocampal MF and CF proteins were identified and quantified with a Dionex Ultimate RSLC nanoUPLC Thermo Fisher Scientific, Waltham, USA online coupled to a QExactive TM Orbitrap TM mass spectrometer Thermo Fisher Scientific, Waltham, USA.

Peptides were loaded onto a pre-column Thermo Scientific PepMap C Chromatography was performed using the following solvents: solvent A water, 0.

The LC eluant was sprayed into the mass spectrometer by means of an easy-spray source Thermo Fisher Scientific, Waltham, USA. Data dependent scans Top 20 were employed to automatically isolate and generate fragment ions by high energy collisional dissociation in the quadrupole mass analyser and measurement of the resulting fragment ions was performed in the Orbitrap analyzer, set at a resolution of Orbitrap raw files were converted to mzXML files using MSConvert software.

The in-house software package iSPY, which was adapted from an earlier version of a peptide quantitation program known as iTracker, was used to identify and quantify peptides 61 , The software was used to convert mzXML to mgf files that were then imported into Mascot and searched against the SwissProt Mouse database November and a decoy database.

In iSPY, Mascot dat output files were run through Percolator for improved identification. Non-unique peptides were discarded. Only peptides with a protein type 1 error of less than 0. The heavy and light peak intensities for each peptide were calculated in iSPY using retention time and sequence information from the MS1 spectra and Mascot search, respectively.

Briefly, the intensities for a pre-specified number of isotopomeric peaks were calculated by scanning through a retention time window spanning a set distance on either side of the maximum intensity value.

The 14 N and 15 N peptide isotopic peaks from the MS1 dataset were used to compare the theoretical mass difference between the heavy and light peptides, and the typical isotopic distribution patterns.

Only quantifiable peptides for which both heavy and a light peak intensities were identified in five replicates were included in the dataset. Samples were obtained, measured and analysed as previously described 28 , Metabolite intensities as well as protein ratios were median-normalised and auto-scaled for statistical analysis.

We improved robustness of our data analyses and increased confidence in significantly altered metabolites and proteins as well as in the subsequent analyses of overrepresented KEGG pathways by only considering the overlap between the two different statistical methods.

Pathway analyses were performed using MetaboAnalyst 64 applying a hypergeometric algorithm for overrepresentation analysis and relative-betweeness centrality for pathway topology analysis. The metabolite pair ratios were calculated as described All data generated or analysed during this study are included in this published article and its Supplementary Information files.

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Article ADS CAS PubMed Google Scholar. Caffeine founds in organic green tea can increase our metabolic rate to aid in thermogenesis and fat oxidization. Antioxidants found in green tea including epigallocatechin gallate EGCG may lower your risk of certain diseases. Organic green tea is packed with powerful antioxidants that can help in the prevention of certain chronic illnesses, type 2 diabetes, and even the flu.

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Like green tea, the active compounds found in ginger may also reduce the risk of certain cancers and the symptoms associated with other diseases like nausea and inflammation. If you enjoyed this article you might also like Have You Ever Wondered How To Increase Metabolism? Antioxidant Foods That Increase Metabolism Foods that increase metabolism are high on our cleanse shopping list.

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