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Wyszukujesz frazę ""Mitochondria, Liver"" wg kryterium: Temat


Tytuł :
Effect of Gloriosa superba linn (EEGS) on mPT and monosodium glutamate-induced proliferative disorder using rat model.
Autorzy :
Olowofolahan AO; Laboratory for Membrane Biochemistry Research and Biotechnology, Department of Biochemistry, College of Medicine, University of Ibadan, Nigeria. Electronic address: .
Olorunsogo OO; Laboratory for Membrane Biochemistry Research and Biotechnology, Department of Biochemistry, College of Medicine, University of Ibadan, Nigeria. Electronic address: .
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Źródło :
Journal of ethnopharmacology [J Ethnopharmacol] 2021 Mar 01; Vol. 267, pp. 113498. Date of Electronic Publication: 2020 Oct 19.
Typ publikacji :
Journal Article
MeSH Terms :
Colchicaceae*/chemistry
Cell Proliferation/*drug effects
Chemical and Drug Induced Liver Injury/*prevention & control
Liver/*drug effects
Membrane Potential, Mitochondrial/*drug effects
Mitochondria, Liver/*drug effects
Plant Extracts/*pharmacology
Prostate/*drug effects
Prostatic Diseases/*prevention & control
Uterine Diseases/*prevention & control
Uterus/*drug effects
Animals ; Apoptosis/drug effects ; Apoptosis Regulatory Proteins/metabolism ; Chemical and Drug Induced Liver Injury/etiology ; Chemical and Drug Induced Liver Injury/metabolism ; Chemical and Drug Induced Liver Injury/pathology ; Disease Models, Animal ; Female ; Hyperplasia ; Lipid Peroxidation/drug effects ; Liver/metabolism ; Liver/pathology ; Male ; Mitochondria, Liver/metabolism ; Mitochondria, Liver/pathology ; Plant Extracts/isolation & purification ; Prostate/metabolism ; Prostate/pathology ; Prostatic Diseases/chemically induced ; Prostatic Diseases/metabolism ; Prostatic Diseases/pathology ; Rats, Wistar ; Signal Transduction ; Sodium Glutamate ; Uterine Diseases/chemically induced ; Uterine Diseases/metabolism ; Uterine Diseases/pathology ; Uterus/metabolism ; Uterus/pathology
Czasopismo naukowe
Tytuł :
Mitochondrial protein adduct and superoxide generation are prerequisites for early activation of c-jun N-terminal kinase within the cytosol after an acetaminophen overdose in mice.
Autorzy :
Nguyen NT; Department of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, Kansas City, KS, 66160, USA.
Du K; Department of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, Kansas City, KS, 66160, USA.
Akakpo JY; Department of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, Kansas City, KS, 66160, USA.
Umbaugh DS; Department of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, Kansas City, KS, 66160, USA.
Jaeschke H; Department of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, Kansas City, KS, 66160, USA.
Ramachandran A; Department of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, Kansas City, KS, 66160, USA. Electronic address: .
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Źródło :
Toxicology letters [Toxicol Lett] 2021 Mar 01; Vol. 338, pp. 21-31. Date of Electronic Publication: 2020 Dec 05.
Typ publikacji :
Journal Article
MeSH Terms :
Acetaminophen*
Drug Overdose*
Chemical and Drug Induced Liver Injury/*enzymology
Cytosol/*enzymology
Hepatocytes/*enzymology
JNK Mitogen-Activated Protein Kinases/*metabolism
Mitochondria, Liver/*enzymology
Mitochondrial Proteins/*metabolism
Superoxides/*metabolism
Animals ; Benzoquinones/metabolism ; Cells, Cultured ; Chemical and Drug Induced Liver Injury/pathology ; Disease Models, Animal ; Enzyme Activation ; Hepatocytes/pathology ; Imines/metabolism ; Male ; Mice, Inbred C57BL ; Mitochondria, Liver/pathology ; Oxidative Stress ; Protein Transport ; Time Factors
Czasopismo naukowe
Tytuł :
Maternal high-fat high-sucrose diet and gestational exercise modulate hepatic fat accumulation and liver mitochondrial respiratory capacity in mothers and male offspring.
Autorzy :
Stevanović-Silva J; Laboratory of Metabolism and Exercise (LaMetEx), Research Centre in Physical Activity, Health and Leisure (CIAFEL), Faculty of Sport, University of Porto, 4200-450, Porto, Portugal. Electronic address: .
Beleza J; Department of Cell Biology, Physiology & Immunology, Faculty of Biology, University of Barcelona, Barcelona, Spain.
Coxito P; Laboratory of Metabolism and Exercise (LaMetEx), Research Centre in Physical Activity, Health and Leisure (CIAFEL), Faculty of Sport, University of Porto, 4200-450, Porto, Portugal.
Pereira S; Laboratory of Metabolism and Exercise (LaMetEx), Research Centre in Physical Activity, Health and Leisure (CIAFEL), Faculty of Sport, University of Porto, 4200-450, Porto, Portugal; CNC - Center for Neuroscience and Cell Biology, UC-Biotech, University of Coimbra, 3060-197 Cantanhede, Portugal.
Rocha H; Newborn Screening, Metabolism and Genetics Unit, Human Genetics Department, National Institute of Health Doutor Ricardo Jorge, 4000-053 Porto, Portugal.
Gaspar TB; Institute for Research and Innovation in Health Sciences (i3S), University of Porto, 4200-135 Porto, Portugal; Cancer Signalling and Metabolism Group, Institute of Molecular Pathology and Immunology of the University of Porto (Ipatimup), 4200-135 Porto, Portugal; Medical Faculty of University of Porto (FMUP), 4200-139 Porto, Portugal; Abel Salazar Biomedical Sciences Institute (ICBAS), University of Porto, 4050-313 Porto, Portugal.
Gärtner F; Institute for Research and Innovation in Health Sciences (i3S), University of Porto, 4200-135 Porto, Portugal; Department of Molecular Pathology and Immunology, Instituto de Ciências Biomédicas Abel Salazar, Universidade do Porto, 4050-313, Porto, Portugal; Glycobiology in Cancer Group, Institute of Molecular Pathology and Immunology of University of Porto (Ipatimup), University of Porto, 4200-135 Porto, Portugal.
Correia R; HEMS - Histology and Electron Microscopy Institute for Research and Innovation in Health Sciences (i3S), University of Porto, 4200-135, Porto, Portugal,; Ipatimup - Institute of Molecular Pathology and Immunology of the University of Porto, 4200-135 Porto, Portugal.
Martins MJ; Institute for Research and Innovation in Health Sciences (i3S), University of Porto, 4200-135 Porto, Portugal; Department of Biomedicine, Biochemistry Unit, Faculty of Medicine, University of Porto, 4200-319 Porto, Portugal.
Guimarães T; Department of Biomedicine, Biochemistry Unit, Faculty of Medicine, University of Porto, 4200-319 Porto, Portugal; Department of Clinical Pathology, São João Hospital Centre, EPE, 4200-319 Porto, Portugal.
Martins S; Department of Clinical Pathology, São João Hospital Centre, EPE, 4200-319 Porto, Portugal; EPIUnit, Institute of Public Health, University of Porto, 4050-091 Porto, Portugal.
Oliveira PJ; CNC - Center for Neuroscience and Cell Biology, UC-Biotech, University of Coimbra, 3060-197 Cantanhede, Portugal.
Ascensão A; Laboratory of Metabolism and Exercise (LaMetEx), Research Centre in Physical Activity, Health and Leisure (CIAFEL), Faculty of Sport, University of Porto, 4200-450, Porto, Portugal.
Magalhães J; Laboratory of Metabolism and Exercise (LaMetEx), Research Centre in Physical Activity, Health and Leisure (CIAFEL), Faculty of Sport, University of Porto, 4200-450, Porto, Portugal.
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Źródło :
Metabolism: clinical and experimental [Metabolism] 2021 Mar; Vol. 116, pp. 154704. Date of Electronic Publication: 2021 Jan 07.
Typ publikacji :
Journal Article; Research Support, Non-U.S. Gov't
MeSH Terms :
Diet, High-Fat*/adverse effects
Liver/*metabolism
Mitochondria, Liver/*metabolism
Physical Conditioning, Animal/*physiology
Prenatal Exposure Delayed Effects/*metabolism
Sucrose/*administration & dosage
Animals ; Cell Respiration/drug effects ; Diabetes, Gestational/metabolism ; Diabetes, Gestational/physiopathology ; Dietary Carbohydrates/adverse effects ; Female ; Lipid Metabolism/drug effects ; Male ; Maternal Nutritional Physiological Phenomena ; Mitochondria, Liver/drug effects ; Mothers ; Pregnancy ; Prenatal Exposure Delayed Effects/physiopathology ; Rats ; Rats, Sprague-Dawley
Czasopismo naukowe
Tytuł :
Mitochondrial Bioenergetic Assays as a Standard Protocol for Toxicological and Metabolic Assessment.
Autorzy :
Teodoro JS; MitoLab, Department of Life Sciences, Center for Neurosciences and Cell Biology of the University of Coimbra, Coimbra, Portugal.
Rolo AP; MitoLab, Department of Life Sciences, Center for Neurosciences and Cell Biology of the University of Coimbra, Coimbra, Portugal.
Palmeira CMM; MitoLab, Department of Life Sciences, Center for Neurosciences and Cell Biology of the University of Coimbra, Coimbra, Portugal. .
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Źródło :
Methods in molecular biology (Clifton, N.J.) [Methods Mol Biol] 2021; Vol. 2240, pp. 231-241.
Typ publikacji :
Journal Article
MeSH Terms :
Biological Assay*
Toxicity Tests*
Energy Metabolism/*drug effects
Mitochondria, Liver/*drug effects
Animals ; Calcium/metabolism ; Membrane Potential, Mitochondrial/drug effects ; Mitochondria, Liver/metabolism ; Mitochondria, Liver/pathology ; Mitochondrial Swelling/drug effects ; Oxygen Consumption/drug effects ; Rats
Czasopismo naukowe
Tytuł :
Transkingdom interactions between Lactobacilli and hepatic mitochondria attenuate western diet-induced diabetes.
Autorzy :
Rodrigues RR; College of Pharmacy, Oregon State University, Corvallis, OR, USA.
Gurung M; Veterinary Medicine, Oregon State University, Corvallis, OR, USA.
Li Z; Veterinary Medicine, Oregon State University, Corvallis, OR, USA.
García-Jaramillo M; College of Public Health and Human Sciences, Oregon State University, Corvallis, OR, USA.
Greer R; Veterinary Medicine, Oregon State University, Corvallis, OR, USA.
Gaulke C; College of Science, Oregon State University, Corvallis, OR, USA.
Bauchinger F; Department of Microbiology and Ecosystem Science, University of Vienna, Vienna, Austria.
You H; Veterinary Medicine, Oregon State University, Corvallis, OR, USA.
Pederson JW; Veterinary Medicine, Oregon State University, Corvallis, OR, USA.
Vasquez-Perez S; Veterinary Medicine, Oregon State University, Corvallis, OR, USA.
White KD; Veterinary Medicine, Oregon State University, Corvallis, OR, USA.
Frink B; Veterinary Medicine, Oregon State University, Corvallis, OR, USA.
Philmus B; College of Pharmacy, Oregon State University, Corvallis, OR, USA.
Jump DB; College of Public Health and Human Sciences, Oregon State University, Corvallis, OR, USA.
Trinchieri G; Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
Berry D; Department of Microbiology and Ecosystem Science, University of Vienna, Vienna, Austria.
Sharpton TJ; College of Science, Oregon State University, Corvallis, OR, USA.
Dzutsev A; Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
Morgun A; College of Pharmacy, Oregon State University, Corvallis, OR, USA. .
Shulzhenko N; Veterinary Medicine, Oregon State University, Corvallis, OR, USA. .
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Źródło :
Nature communications [Nat Commun] 2021 Jan 04; Vol. 12 (1), pp. 101. Date of Electronic Publication: 2021 Jan 04.
Typ publikacji :
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
MeSH Terms :
Diet, Western*
Diabetes Mellitus, Type 2/*etiology
Diabetes Mellitus, Type 2/*microbiology
Lactobacillus/*metabolism
Mitochondria, Liver/*metabolism
Animals ; Bilirubin/blood ; Diabetes Mellitus, Type 2/genetics ; Gastrointestinal Microbiome ; Gene Expression Regulation ; Glucose/metabolism ; Glutathione/blood ; Glutathione/metabolism ; Humans ; Lipid Metabolism ; Male ; Metabolomics ; Mice, Inbred C57BL ; Mitochondria, Liver/ultrastructure ; Reproducibility of Results ; Transcriptome/genetics
Czasopismo naukowe
Tytuł :
Energy disorders caused by mitochondrial dysfunction contribute to α-amatoxin-induced liver function damage and liver failure.
Autorzy :
Chen X; Chinese Center for Disease Control and Prevention, Beijing, Beijing, China. Electronic address: .
Shao B; Beijing Center for Disease Control and Prevention Beijing, China. Electronic address: .
Yu C; Yunnan Chuxiong People's Hospital, Chuxiong, Yunnan, China. Electronic address: .
Yao Q; Yunnan Chuxiong People's Hospital, Chuxiong, Yunnan, China. Electronic address: .
Ma P; Chinese Center for Disease Control and Prevention, Beijing, Beijing, China. Electronic address: .
Li H; Chinese Center for Disease Control and Prevention, Beijing, Beijing, China. Electronic address: .
Li B; Chinese Center for Disease Control and Prevention, Beijing, Beijing, China. Electronic address: .
Sun C; Chinese Center for Disease Control and Prevention, 29th Nanwei Road, Xicheng District, Beijing, 102206, China. Electronic address: .
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Źródło :
Toxicology letters [Toxicol Lett] 2021 Jan 01; Vol. 336, pp. 68-79. Date of Electronic Publication: 2020 Oct 22.
Typ publikacji :
Journal Article
MeSH Terms :
Amanitins*
Energy Metabolism*
Chemical and Drug Induced Liver Injury/*metabolism
Liver/*metabolism
Liver Failure/*metabolism
Mitochondria, Liver/*metabolism
Mushroom Poisoning/*metabolism
Animals ; Cell Line ; Chemical and Drug Induced Liver Injury/etiology ; Chemical and Drug Induced Liver Injury/pathology ; Disease Models, Animal ; Humans ; Liver/pathology ; Liver Failure/chemically induced ; Liver Failure/pathology ; Metabolomics ; Mice, Inbred BALB C ; Mitochondria, Liver/pathology ; Mushroom Poisoning/etiology ; Mushroom Poisoning/pathology ; Time Factors
Czasopismo naukowe
Tytuł :
The mitochondria-targeted derivative of the classical uncoupler of oxidative phosphorylation carbonyl cyanide m-chlorophenylhydrazone is an effective mitochondrial recoupler.
Autorzy :
Iaubasarova IR; Belozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, Moscow, Russia.; Faculty of Chemistry, Lomonosov Moscow State University, Moscow, Russia.
Khailova LS; Belozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, Moscow, Russia.
Firsov AM; Belozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, Moscow, Russia.
Grivennikova VG; Faculty of Biology, Lomonosov Moscow State University, Moscow, Russia.
Kirsanov RS; Belozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, Moscow, Russia.
Korshunova GA; Belozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, Moscow, Russia.
Kotova EA; Belozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, Moscow, Russia.
Antonenko YN; Belozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, Moscow, Russia.
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Źródło :
PloS one [PLoS One] 2020 Dec 30; Vol. 15 (12), pp. e0244499. Date of Electronic Publication: 2020 Dec 30 (Print Publication: 2020).
Typ publikacji :
Journal Article; Research Support, Non-U.S. Gov't
MeSH Terms :
Carbonyl Cyanide m-Chlorophenyl Hydrazone/*pharmacology
Mitochondria, Liver/*drug effects
Oxidative Coupling/*drug effects
Oxidative Phosphorylation/*drug effects
Animals ; Carbonyl Cyanide m-Chlorophenyl Hydrazone/analogs & derivatives ; Cattle ; Ketocholesterols/pharmacology ; Membrane Potentials/drug effects ; Membrane Potentials/physiology ; Mitochondria, Liver/metabolism ; Rats ; Uncoupling Agents/pharmacology
Czasopismo naukowe
Tytuł :
CDKN2A/p16INK4a suppresses hepatic fatty acid oxidation through the AMPKα2-SIRT1-PPARα signaling pathway.
Autorzy :
Deleye Y; Univ. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011-EGID, Lille, France.
Cotte AK; Univ. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011-EGID, Lille, France.
Hannou SA; Univ. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011-EGID, Lille, France.
Hennuyer N; Univ. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011-EGID, Lille, France.
Bernard L; Univ. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011-EGID, Lille, France.
Derudas B; Univ. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011-EGID, Lille, France.
Caron S; Univ. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011-EGID, Lille, France.
Legry V; Univ. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011-EGID, Lille, France.
Vallez E; Univ. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011-EGID, Lille, France.
Dorchies E; Univ. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011-EGID, Lille, France.
Martin N; Univ. Lille, CNRSInstitut Pasteur de Lille, UMR 8161-M3T-Mechanisms of Tumorigenesis and Target Therapies, Lille, France.
Lancel S; Univ. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011-EGID, Lille, France.
Annicotte JS; Univ. Lille, CNRSCHU Lille, Institut Pasteur de Lille, UMR 8199-EGID, Lille, France.
Bantubungi K; Univ. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011-EGID, Lille, France.
Pourtier A; Univ. Lille, CNRSInstitut Pasteur de Lille, UMR 8161-M3T-Mechanisms of Tumorigenesis and Target Therapies, Lille, France.
Raverdy V; Univ. Lille, Inserm, CHU Lille, UMR 1190-EGID, Lille, France.
Pattou F; Univ. Lille, Inserm, CHU Lille, UMR 1190-EGID, Lille, France.
Lefebvre P; Univ. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011-EGID, Lille, France.
Abbadie C; Univ. Lille, CNRSInstitut Pasteur de Lille, UMR 8161-M3T-Mechanisms of Tumorigenesis and Target Therapies, Lille, France.
Staels B; Univ. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011-EGID, Lille, France.
Haas JT; Univ. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011-EGID, Lille, France.
Paumelle R; Univ. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011-EGID, Lille, France. Electronic address: .
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Źródło :
The Journal of biological chemistry [J Biol Chem] 2020 Dec 11; Vol. 295 (50), pp. 17310-17322. Date of Electronic Publication: 2020 Oct 09.
Typ publikacji :
Journal Article; Research Support, Non-U.S. Gov't
MeSH Terms :
Signal Transduction*
AMP-Activated Protein Kinases/*metabolism
Cyclin-Dependent Kinase Inhibitor p16/*metabolism
Fatty Acids/*metabolism
Liver/*metabolism
Mitochondria, Liver/*metabolism
PPAR alpha/*metabolism
Sirtuin 1/*metabolism
AMP-Activated Protein Kinases/genetics ; Animals ; Cyclin-Dependent Kinase Inhibitor p16/genetics ; Fatty Acids/genetics ; Genome-Wide Association Study ; Humans ; Lipid Droplets/metabolism ; Mice ; Mice, Knockout ; Mitochondria, Liver/genetics ; Obesity/genetics ; Obesity/metabolism ; Oxidation-Reduction ; PPAR alpha/genetics ; Sirtuin 1/genetics
Czasopismo naukowe
Tytuł :
9-PAHSA Prevents Mitochondrial Dysfunction and Increases the Viability of Steatotic Hepatocytes.
Autorzy :
Schultz Moreira AR; Department of Gastroenterology and Hepatology, University Hospital Essen, University Duisburg-Essen, 45147 Essen, Germany.
Rüschenbaum S; Department of Gastroenterology and Hepatology, University Hospital Essen, University Duisburg-Essen, 45147 Essen, Germany.
Schefczyk S; Department of Gastroenterology and Hepatology, University Hospital Essen, University Duisburg-Essen, 45147 Essen, Germany.
Hendgen-Cotta U; West German Heart and Vascular Center, Department of Cardiology and Vascular Medicine, University Hospital Essen, University of Duisburg-Essen, 45147 Essen, Germany.
Rassaf T; West German Heart and Vascular Center, Department of Cardiology and Vascular Medicine, University Hospital Essen, University of Duisburg-Essen, 45147 Essen, Germany.
Broering R; Department of Gastroenterology and Hepatology, University Hospital Essen, University Duisburg-Essen, 45147 Essen, Germany.
Hardtke-Wolenski M; Department of Gastroenterology and Hepatology, University Hospital Essen, University Duisburg-Essen, 45147 Essen, Germany.; Department of Gastroenterology, Hepatology & Endocrinology, Hannover Medical School, 30625 Hannover, Germany.
Buitrago-Molina LE; Department of Gastroenterology and Hepatology, University Hospital Essen, University Duisburg-Essen, 45147 Essen, Germany.; Department of Gastroenterology, Hepatology & Endocrinology, Hannover Medical School, 30625 Hannover, Germany.
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Źródło :
International journal of molecular sciences [Int J Mol Sci] 2020 Nov 05; Vol. 21 (21). Date of Electronic Publication: 2020 Nov 05.
Typ publikacji :
Journal Article
MeSH Terms :
Fatty Liver/*pathology
Hepatocytes/*drug effects
Mitochondria, Liver/*drug effects
Mitochondrial Diseases/*prevention & control
Palmitic Acid/*pharmacology
Stearic Acids/*pharmacology
Animals ; Cell Survival/drug effects ; Cells, Cultured ; Cytoprotection/drug effects ; Fatty Liver/metabolism ; Fatty Liver/physiopathology ; Hep G2 Cells ; Hepatocytes/pathology ; Hepatocytes/physiology ; Humans ; Liver/drug effects ; Liver/pathology ; Mice ; Mice, Inbred C57BL ; Mitochondria, Liver/physiology ; Mitochondrial Diseases/etiology
Czasopismo naukowe
Tytuł :
IL-17a exacerbates hepatic ischemia-reperfusion injury in fatty liver by promoting neutrophil infiltration and mitochondria-driven apoptosis.
Autorzy :
Yang X; Department of Surgery, HKU-SZH & Faculty of Medicine, The University of Hong Kong, Hong Kong, China.
Li C; Department of Surgery, HKU-SZH & Faculty of Medicine, The University of Hong Kong, Hong Kong, China.; Department of Liver Surgery, First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Ng KT; Department of Surgery, HKU-SZH & Faculty of Medicine, The University of Hong Kong, Hong Kong, China.
Liu J; Department of Surgery, HKU-SZH & Faculty of Medicine, The University of Hong Kong, Hong Kong, China.; Department of Surgery, Beijing Tsinghua Changgung Hospital, Tsinghua University, Beijing, China.
Liu H; Department of Surgery, HKU-SZH & Faculty of Medicine, The University of Hong Kong, Hong Kong, China.
Zhang W; Department of Surgery, HKU-SZH & Faculty of Medicine, The University of Hong Kong, Hong Kong, China.
Xiao F; Department of Pathology, Faculty of Medicine, The University of Hong Kong, Hong Kong, China.
Li X; Department of Liver Surgery, First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Lo CM; Department of Surgery, HKU-SZH & Faculty of Medicine, The University of Hong Kong, Hong Kong, China.
Lu L; Department of Pathology, Faculty of Medicine, The University of Hong Kong, Hong Kong, China.
Man K; Department of Surgery, HKU-SZH & Faculty of Medicine, The University of Hong Kong, Hong Kong, China.
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Źródło :
Journal of leukocyte biology [J Leukoc Biol] 2020 Nov; Vol. 108 (5), pp. 1603-1613. Date of Electronic Publication: 2020 Jun 12.
Typ publikacji :
Journal Article; Research Support, Non-U.S. Gov't
MeSH Terms :
Neutrophil Infiltration*
Apoptosis/*immunology
Fatty Liver/*immunology
Interleukin-17/*immunology
Mitochondria, Liver/*immunology
Neutrophils/*immunology
Reperfusion Injury/*immunology
Animals ; Fatty Liver/pathology ; Female ; Humans ; Male ; Mitochondria, Liver/pathology ; Neutrophils/pathology ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury/pathology
Czasopismo naukowe
Tytuł :
Flavonoids modulate liposomal membrane structure, regulate mitochondrial membrane permeability and prevent erythrocyte oxidative damage.
Autorzy :
Veiko AG; Department of Biochemistry, Yanka Kupala State University of Grodno, 230030 Grodno, Belarus.
Sekowski S; Faculty of Biology, University of Bialystok, Ciolkowskiego 1J, 15-245 Bialystok, Poland.
Lapshina EA; Department of Biochemistry, Yanka Kupala State University of Grodno, 230030 Grodno, Belarus.
Wilczewska AZ; Faculty of Chemistry, University of Białystok, Ciolkowskiego 1K, 15-245 Bialystok, Poland.
Markiewicz KH; Faculty of Chemistry, University of Białystok, Ciolkowskiego 1K, 15-245 Bialystok, Poland.
Zamaraeva M; Faculty of Biology, University of Bialystok, Ciolkowskiego 1J, 15-245 Bialystok, Poland.
Zhao HC; Institute of Biomechanics and Medical Engineering, Tsinghua University, 100084 Beijing, PR China.
Zavodnik IB; Department of Biochemistry, Yanka Kupala State University of Grodno, 230030 Grodno, Belarus. Electronic address: .
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Źródło :
Biochimica et biophysica acta. Biomembranes [Biochim Biophys Acta Biomembr] 2020 Nov 01; Vol. 1862 (11), pp. 183442. Date of Electronic Publication: 2020 Aug 16.
Typ publikacji :
Journal Article; Research Support, Non-U.S. Gov't
MeSH Terms :
Erythrocytes/*chemistry
Flavonoids/*chemistry
Mitochondria, Liver/*chemistry
Mitochondrial Membranes/*chemistry
Animals ; Erythrocytes/metabolism ; Flavonoids/pharmacology ; Liposomes ; Mitochondria, Liver/metabolism ; Mitochondrial Membranes/metabolism ; Oxidation-Reduction ; Permeability ; Rats ; tert-Butylhydroperoxide/chemistry ; tert-Butylhydroperoxide/pharmacology
Czasopismo naukowe
Tytuł :
Glutamate dehydrogenase as a biomarker for mitotoxicity; insights from furosemide hepatotoxicity in the mouse.
Autorzy :
Church RJ; Institute for Drug Safety Sciences, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America.; Division of Pharmacotherapy and Experimental Therapeutics, Eshelman School of Pharmacy, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America.
Schomaker SJ; Pfizer Inc., Groton, Connecticut, United States of America.
Eaddy JS; Institute for Drug Safety Sciences, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America.
Boucher GG; Pfizer Inc., Groton, Connecticut, United States of America.
Kreeger JM; Pfizer Inc., Groton, Connecticut, United States of America.
Aubrecht J; Pfizer Inc., Groton, Connecticut, United States of America.
Watkins PB; Institute for Drug Safety Sciences, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America.; Division of Pharmacotherapy and Experimental Therapeutics, Eshelman School of Pharmacy, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America.
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Źródło :
PloS one [PLoS One] 2020 Oct 09; Vol. 15 (10), pp. e0240562. Date of Electronic Publication: 2020 Oct 09 (Print Publication: 2020).
Typ publikacji :
Journal Article; Research Support, Non-U.S. Gov't
MeSH Terms :
Mitochondria, Liver*/drug effects
Mitochondria, Liver*/metabolism
Alanine Transaminase/*blood
Chemical and Drug Induced Liver Injury/*metabolism
Furosemide/*adverse effects
Glutamate Dehydrogenase/*blood
Mitophagy/*drug effects
Acetaminophen/adverse effects ; Animals ; Biomarkers/blood ; Hepatocytes/metabolism ; Hepatocytes/pathology ; Liver/metabolism ; Liver/pathology ; Male ; Mice ; Mice, Inbred C57BL
Czasopismo naukowe
Tytuł :
miR-29a Modulates GSK3β/SIRT1-Linked Mitochondrial Proteostatic Stress to Ameliorate Mouse Non-Alcoholic Steatohepatitis.
Autorzy :
Yang YL; Department of Anesthesiology, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung 833, Taiwan.
Wang PW; Department of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung 833, Taiwan.; Center for Mitochondrial Research and Medicine, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung 833, Taiwan.
Wang FS; Center for Mitochondrial Research and Medicine, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung 833, Taiwan.; Core Laboratory for Phenomics & Diagnostics, Department of Medical Research, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung 833, Taiwan.
Lin HY; Department of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung 833, Taiwan.; Center for Mitochondrial Research and Medicine, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung 833, Taiwan.; Research Assistant Center, Show Chwan Memorial Hospital, Changhua 500, Taiwan.
Huang YH; Department of Pediatrics, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung 833, Taiwan.
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Źródło :
International journal of molecular sciences [Int J Mol Sci] 2020 Sep 19; Vol. 21 (18). Date of Electronic Publication: 2020 Sep 19.
Typ publikacji :
Journal Article
MeSH Terms :
Proteostasis*
Glycogen Synthase Kinase 3 beta/*metabolism
MicroRNAs/*biosynthesis
Mitochondria, Liver/*metabolism
Non-alcoholic Fatty Liver Disease/*metabolism
Non-alcoholic Fatty Liver Disease/*prevention & control
Sirtuin 1/*metabolism
Animals ; Glycogen Synthase Kinase 3 beta/genetics ; Mice ; Mice, Transgenic ; MicroRNAs/genetics ; Mitochondria, Liver/genetics ; Mitochondria, Liver/pathology ; Non-alcoholic Fatty Liver Disease/genetics ; Non-alcoholic Fatty Liver Disease/pathology ; Sirtuin 1/genetics ; Unfolded Protein Response
Czasopismo naukowe
Tytuł :
Dendrobium nobile Lindl. alkaloids-mediated protection against CCl 4- induced liver mitochondrial oxidative damage is dependent on the activation of Nrf2 signaling pathway.
Autorzy :
Zhou J; Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnocentric of Ministry of Education, Zunyi Medical University, Zunyi, Guizhou, 563003, China.
Zhang Y; Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnocentric of Ministry of Education, Zunyi Medical University, Zunyi, Guizhou, 563003, China.
Li S; Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnocentric of Ministry of Education, Zunyi Medical University, Zunyi, Guizhou, 563003, China.
Zhou Q; Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnocentric of Ministry of Education, Zunyi Medical University, Zunyi, Guizhou, 563003, China.
Lu Y; Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnocentric of Ministry of Education, Zunyi Medical University, Zunyi, Guizhou, 563003, China.
Shi J; Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnocentric of Ministry of Education, Zunyi Medical University, Zunyi, Guizhou, 563003, China.
Liu J; Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnocentric of Ministry of Education, Zunyi Medical University, Zunyi, Guizhou, 563003, China.
Wu Q; Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnocentric of Ministry of Education, Zunyi Medical University, Zunyi, Guizhou, 563003, China. Electronic address: .
Zhou S; Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnocentric of Ministry of Education, Zunyi Medical University, Zunyi, Guizhou, 563003, China. Electronic address: .
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Źródło :
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie [Biomed Pharmacother] 2020 Sep; Vol. 129, pp. 110351. Date of Electronic Publication: 2020 Jun 11.
Typ publikacji :
Journal Article
MeSH Terms :
Carbon Tetrachloride*
Dendrobium*/chemistry
Alkaloids/*pharmacology
Antioxidants/*pharmacology
Chemical and Drug Induced Liver Injury/*prevention & control
Liver/*drug effects
Mitochondria, Liver/*drug effects
NF-E2-Related Factor 2/*metabolism
Oxidative Stress/*drug effects
Reactive Oxygen Species/*metabolism
Alkaloids/isolation & purification ; Animals ; Antioxidants/isolation & purification ; Apoptosis/drug effects ; Chemical and Drug Induced Liver Injury/etiology ; Chemical and Drug Induced Liver Injury/metabolism ; Chemical and Drug Induced Liver Injury/pathology ; DNA Damage/drug effects ; Disease Models, Animal ; Liver/metabolism ; Liver/pathology ; Male ; Mice, Knockout ; Mitochondria, Liver/metabolism ; Mitochondria, Liver/pathology ; NF-E2-Related Factor 2/deficiency ; NF-E2-Related Factor 2/genetics ; Signal Transduction
Czasopismo naukowe
Tytuł :
The effect of Ginsenoside Rg1 in hepatic ischemia reperfusion (I/R) injury ameliorates ischemia-reperfusion-induced liver injury by inhibiting apoptosis.
Autorzy :
Lin J; Organ Transplantation Center, The First Affiliated Hospital, Kunming Medical University, Kunming, China.
Huang HF; Organ Transplantation Center, The First Affiliated Hospital, Kunming Medical University, Kunming, China.
Yang SK; Organ Transplantation Center, The First Affiliated Hospital, Kunming Medical University, Kunming, China.
Duan J; Organ Transplantation Center, The First Affiliated Hospital, Kunming Medical University, Kunming, China.
Qu SM; Organ Transplantation Center, The First Affiliated Hospital, Kunming Medical University, Kunming, China.
Yuan B; Organ Transplantation Center, The First Affiliated Hospital, Kunming Medical University, Kunming, China.
Zeng Z; Organ Transplantation Center, The First Affiliated Hospital, Kunming Medical University, Kunming, China. Electronic address: .
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Źródło :
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie [Biomed Pharmacother] 2020 Sep; Vol. 129, pp. 110398. Date of Electronic Publication: 2020 Jun 27.
Typ publikacji :
Journal Article
MeSH Terms :
Apoptosis/*drug effects
Ginsenosides/*pharmacology
Hepatocytes/*drug effects
Liver/*drug effects
Liver Diseases/*prevention & control
Mitochondria, Liver/*drug effects
Reperfusion Injury/*prevention & control
Animals ; Cell Proliferation/drug effects ; Cells, Cultured ; Cyclophilin D/genetics ; Cyclophilin D/metabolism ; Disease Models, Animal ; Hepatocytes/metabolism ; Hepatocytes/ultrastructure ; Liver/metabolism ; Liver/ultrastructure ; Liver Diseases/genetics ; Liver Diseases/metabolism ; Liver Diseases/pathology ; Male ; Membrane Potential, Mitochondrial/drug effects ; Mitochondria, Liver/metabolism ; Mitochondria, Liver/ultrastructure ; Rats, Sprague-Dawley ; Reperfusion Injury/genetics ; Reperfusion Injury/metabolism ; Reperfusion Injury/pathology
Czasopismo naukowe
Tytuł :
Undesirable effects of chemical inhibitors of NAD(P) transhydrogenase on mitochondrial respiratory function.
Autorzy :
Bicego R; Department of Clinical Pathology, Faculty of Medical Sciences, University of Campinas (UNICAMP), Campinas, SP, Brazil.
Francisco A; Department of Clinical Pathology, Faculty of Medical Sciences, University of Campinas (UNICAMP), Campinas, SP, Brazil. Electronic address: .
Ruas JS; Department of Clinical Pathology, Faculty of Medical Sciences, University of Campinas (UNICAMP), Campinas, SP, Brazil.
Siqueira-Santos ES; Department of Clinical Pathology, Faculty of Medical Sciences, University of Campinas (UNICAMP), Campinas, SP, Brazil.
Castilho RF; Department of Clinical Pathology, Faculty of Medical Sciences, University of Campinas (UNICAMP), Campinas, SP, Brazil. Electronic address: .
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Źródło :
Archives of biochemistry and biophysics [Arch Biochem Biophys] 2020 Oct 15; Vol. 692, pp. 108535. Date of Electronic Publication: 2020 Aug 08.
Typ publikacji :
Journal Article; Research Support, Non-U.S. Gov't
MeSH Terms :
Enzyme Inhibitors/*pharmacology
Mitochondria, Liver/*enzymology
NADP Transhydrogenase, AB-Specific/*antagonists & inhibitors
NADP Transhydrogenase, AB-Specific/*metabolism
Oxygen Consumption/*drug effects
Animals ; Enzyme Inhibitors/chemistry ; Female ; Mice ; Mice, Knockout ; Mitochondria, Liver/genetics ; Mitochondrial Proteins/antagonists & inhibitors ; Mitochondrial Proteins/genetics ; Mitochondrial Proteins/metabolism ; NADP Transhydrogenase, AB-Specific/genetics ; Oxygen Consumption/genetics
Czasopismo naukowe
Tytuł :
Bicarbonate suppresses mitochondrial membrane depolarization induced by conventional uncouplers.
Autorzy :
Khailova LS; Belozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, Leninskie Gory 1/40, Moscow, 119991, Russia.
Vygodina TV; Belozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, Leninskie Gory 1/40, Moscow, 119991, Russia.
Lomakina GY; Faculty of Chemistry, Lomonosov Moscow State University, Leninskie Gory 1/3, Moscow, 119991, Russia; Bauman Moscow State Technical University, Baumanskaya 2-ya, 5/1, Moscow, 105005, Russia.
Kotova EA; Belozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, Leninskie Gory 1/40, Moscow, 119991, Russia.
Antonenko YN; Belozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, Leninskie Gory 1/40, Moscow, 119991, Russia. Electronic address: .
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Źródło :
Biochemical and biophysical research communications [Biochem Biophys Res Commun] 2020 Sep 10; Vol. 530 (1), pp. 29-34. Date of Electronic Publication: 2020 Jul 28.
Typ publikacji :
Journal Article; Research Support, Non-U.S. Gov't
MeSH Terms :
Bicarbonates/*metabolism
Membrane Potential, Mitochondrial/*drug effects
Mitochondria, Liver/*drug effects
Uncoupling Agents/*pharmacology
2,4-Dinitrophenol/pharmacology ; Adenosine Triphosphate/metabolism ; Animals ; Carbonyl Cyanide m-Chlorophenyl Hydrazone/pharmacology ; Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone/pharmacology ; Mitochondria, Liver/metabolism ; Mitochondrial Membranes/drug effects ; Mitochondrial Membranes/metabolism ; Rats
Czasopismo naukowe
Tytuł :
[Features of free radical processes in the liver of rats with a nutrient imbalance].
Autorzy :
Voloshchuk ON; Fedkovych Chernovtsi National University, Institute of Biology, Chemistry and Bioresources, Department of Biochemistry and Biotechnology, Chernovtsi, Ukraine.
Stus YV; Fedkovych Chernovtsi National University, Institute of Biology, Chemistry and Bioresources, Department of Biochemistry and Biotechnology, Chernovtsi, Ukraine.
Kopylchuk GP; Fedkovych Chernovtsi National University, Institute of Biology, Chemistry and Bioresources, Department of Biochemistry and Biotechnology, Chernovtsi, Ukraine.
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Transliterated Title :
Intensivnost' svobodnoradikal'nogo okisleniia biomolekul mitokhondriĭ gepatotsitov pri nutrientnom disbalanse.
Źródło :
Biomeditsinskaia khimiia [Biomed Khim] 2020 Sep; Vol. 66 (5), pp. 386-391.
Typ publikacji :
Journal Article
MeSH Terms :
Liver*/metabolism
Mitochondria, Liver*/metabolism
Animals ; Free Radicals/metabolism ; Lipid Peroxidation ; Nutrients ; Rats
Czasopismo naukowe
Tytuł :
Cr(VI)-induced overactive mitophagy contributes to mitochondrial loss and cytotoxicity in L02 hepatocytes.
Autorzy :
Zhang Y; Department of Health Toxicology, Xiangya School of Public Health, Central South University, Changsha 410078, PR China.
Bian H; Shajing Health Inspection Institute of Baoan District, Shenzhen 518104, PR China.
Ma Y; Department of Health Toxicology, Xiangya School of Public Health, Central South University, Changsha 410078, PR China.
Xiao Y; Department of Health Toxicology, Xiangya School of Public Health, Central South University, Changsha 410078, PR China.
Xiao F; Department of Health Toxicology, Xiangya School of Public Health, Central South University, Changsha 410078, PR China.
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Źródło :
The Biochemical journal [Biochem J] 2020 Jul 31; Vol. 477 (14), pp. 2607-2619.
Typ publikacji :
Journal Article; Research Support, Non-U.S. Gov't
MeSH Terms :
Chromium/*toxicity
Hepatocytes/*drug effects
Mitochondria, Liver/*drug effects
Mitophagy/*drug effects
Adenosine Triphosphate/metabolism ; Autophagosomes/drug effects ; Autophagy-Related Protein 5/genetics ; Cell Death/drug effects ; Cell Line ; Energy Metabolism/drug effects ; Hepatocytes/metabolism ; Hepatocytes/pathology ; Humans ; Mitochondria, Liver/metabolism ; Mitochondria, Liver/pathology ; Reactive Oxygen Species/metabolism
Czasopismo naukowe
Tytuł :
Effect of a post-translational modification mimic on protein translocation through a nanopore.
Autorzy :
Hoogerheide DP; Center for Neutron Research, National Institute of Standards and Technology, Gaithersburg, MD 20899, USA. .
Gurnev PA; Section on Molecular Transport, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA.
Rostovtseva TK; Section on Molecular Transport, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA.
Bezrukov SM; Section on Molecular Transport, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA.
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Źródło :
Nanoscale [Nanoscale] 2020 May 28; Vol. 12 (20), pp. 11070-11078.
Typ publikacji :
Journal Article
MeSH Terms :
Mitochondria, Liver*/chemistry
Mitochondria, Liver*/metabolism
Mitochondrial Membranes*/chemistry
Mitochondrial Membranes*/metabolism
Nanopores*
Protein Processing, Post-Translational*
alpha-Synuclein*/chemistry
alpha-Synuclein*/metabolism
Animals ; Protein Transport ; Rats
Czasopismo naukowe

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