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Article ; Online: Versatile roles of cysteine persulfides in tumor biology.

Borbényi-Galambos, Klaudia / Czikora, Ágnes / Erdélyi, Katalin / Nagy, Péter

2024 Volume 79, Page(s) 102440

Abstract: Rewiring the transsulfuration pathway is recognized as a rapid adaptive metabolic response to environmental conditions in cancer cells to support their increased cysteine demand and to produce Reactive Sulfur Species (RSS) including hydrogen sulfide ( ... ...

Abstract	Rewiring the transsulfuration pathway is recognized as a rapid adaptive metabolic response to environmental conditions in cancer cells to support their increased cysteine demand and to produce Reactive Sulfur Species (RSS) including hydrogen sulfide (H
MeSH term(s)	Cysteine/analogs & derivatives ; Epithelial-Mesenchymal Transition ; Cell Survival ; Sulfur ; Biology ; Disulfides
Chemical Substances	cysteine persulfide (3RZ74WA9J2) ; Cysteine (K848JZ4886) ; Sulfur (70FD1KFU70) ; Disulfides
Language	English
Publishing date	2024-02-28
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1439176-4
ISSN	1879-0402 ; 1367-5931
ISSN (online)	1879-0402
ISSN	1367-5931
DOI	10.1016/j.cbpa.2024.102440
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Zs.A 4986: Show issues

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Article ; Online: Cystathionine β-synthase overexpression drives metastatic dissemination in pancreatic ductal adenocarcinoma via inducing epithelial-to-mesenchymal transformation of cancer cells.

Czikora, Ágnes / Erdélyi, Katalin / Ditrói, Tamás / Szántó, Noémi / Jurányi, Eszter Petra / Szanyi, Szilárd / Tóvári, József / Strausz, Tamás / Nagy, Péter

Redox biology

2022 Volume 57, Page(s) 102505

Abstract: Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest of all cancer types with a constant rise in global incidence. Therefore, better understanding of PDAC biology, in order to design more efficient diagnostic and treatment modalities, is a ... ...

Abstract	Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest of all cancer types with a constant rise in global incidence. Therefore, better understanding of PDAC biology, in order to design more efficient diagnostic and treatment modalities, is a priority. Here we found that the expression levels of cystathionine β-synthase (CBS), a transsulfuration enzyme, is markedly elevated in metastatic PDAC cells compared to cell lines isolated from non-metastatic primary tumors. On human immunohistochemical samples from PDAC patients we also found higher CBS staining in cancerous ductal cells compared to in non-tumor tissue, which was further elevated in the lymph node metastasis of the same patients. In mice, orthotopically injected CBS-silenced T3M4 cells induced fewer liver metastases compared to control cells indicating important roles for CBS in PDAC cancer cell invasion and malignant transformation. Wound healing and colony formation assays in cell culture confirmed that CBS-deficient metastatic T3M4 and non-metastatic BxPC3 primary tumor cells migrate slower and have impaired anchorage-independent growth capacities compared to control T3M4 cells. CBS silencing in T3M4 cells lowered WNT5a and SNAI1 gene expression down to levels that were observed in BxPC3 cells as well as resulted in an increase in E-cadherin and a decrease in Vimentin signals in mouse tumors when injected orthotopically. These observations suggested a primary role for the epithelial to mesenchymal transformation of cancer cells in CBS-mediated tumor aggressiveness. Under normal conditions, STAT3, an upstream regulator of Wnt signaling pathways, was less phosphorylated and more oxidized in shCBS T3M4 and BxPC3 compared to control T3M4 cells, which is consistent with decreased transcriptional activity at lower CBS levels due to less protection against oxidation. Sulfur metabolome analyses suggested that this CBS-mediated protection against oxidative modifications is likely to be related to persulfide/sulfide producing activities of the enzyme rather than its canonical function to produce cystathionine for cysteine synthesis. Taken together, CBS overexpression through regulation of the EMT plays a significant role in PDAC cancer cell invasion and metastasis.
Language	English
Publishing date	2022-10-10
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2701011-9
ISSN	2213-2317 ; 2213-2317
ISSN (online)	2213-2317
ISSN	2213-2317
DOI	10.1016/j.redox.2022.102505
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Article ; Online: The role of glutamate oxaloacetate transaminases in sulfite biosynthesis and H

Mellis, Anna-Theresa / Misko, Albert L / Arjune, Sita / Liang, Ye / Erdélyi, Katalin / Ditrói, Tamás / Kaczmarek, Alexander T / Nagy, Peter / Schwarz, Guenter

Redox biology

2020 Volume 38, Page(s) 101800

Abstract: Molybdenum cofactor deficiency and isolated sulfite oxidase deficiency are two rare genetic disorders that are caused by impairment of the mitochondrial enzyme sulfite oxidase. Sulfite oxidase is catalyzing the terminal reaction of cellular cysteine ... ...

Abstract	Molybdenum cofactor deficiency and isolated sulfite oxidase deficiency are two rare genetic disorders that are caused by impairment of the mitochondrial enzyme sulfite oxidase. Sulfite oxidase is catalyzing the terminal reaction of cellular cysteine catabolism, the oxidation of sulfite to sulfate. Absence of sulfite oxidase leads to the accumulation of sulfite, which has been identified as a cellular toxin. However, the molecular pathways leading to the production of sulfite are still not completely understood. In order to identify novel treatment options for both disorders, the understanding of cellular cysteine catabolism - and its alterations upon loss of sulfite oxidase - is of utmost importance. Here we applied a new detection method of sulfite in cellular extracts to dissect the contribution of cytosolic and mitochondrial glutamate oxaloacetate transaminase (GOT) in the transformation of cysteine sulfinic acid to sulfite and pyruvate. We found that the cytosolic isoform GOT1 is primarily responsible for the production of sulfite. Moreover, loss of sulfite oxidase activity results in the accumulation of sulfite, H
MeSH term(s)	Glutamates ; Oxaloacetates ; Sulfite Oxidase/genetics ; Sulfites ; Transaminases/genetics
Chemical Substances	Glutamates ; Oxaloacetates ; Sulfites ; Sulfite Oxidase (EC 1.8.3.1) ; Transaminases (EC 2.6.1.-)
Language	English
Publishing date	2020-11-24
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2701011-9
ISSN	2213-2317 ; 2213-2317
ISSN (online)	2213-2317
ISSN	2213-2317
DOI	10.1016/j.redox.2020.101800
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Article ; Online: Role of poly(ADP-ribosyl)ation in a 'two-hit' model of hypoxia and oxidative stress in human A549 epithelial cells in vitro.

Erdélyi, Katalin / Pacher, Pál / Virág, László / Szabó, Csaba

International journal of molecular medicine

2013 Volume 32, Issue 2, Page(s) 339–346

Abstract: A preceding hypoxic insult can sensitize the cells or the organism to a subsequent, second insult. The aim of the present study was to investigate the molecular mechanism of this phenomenon (often termed 'two-hit' injury paradigm), in an in vitro model ... ...

Abstract	A preceding hypoxic insult can sensitize the cells or the organism to a subsequent, second insult. The aim of the present study was to investigate the molecular mechanism of this phenomenon (often termed 'two-hit' injury paradigm), in an in vitro model of hypoxia/oxidative stress injury in A549 epithelial cells, with special emphasis on the role of the nuclear enzyme poly(ADP-ribose) polymerase-1 (PARP-1) in the process. Pre-exposure of the cells to 24 h hypoxia significantly reduced intracellular glutathione (GSH) levels, reduced mitochondrial activity and adenosine triphosphate (ATP) levels. However pre-exposure to hypoxia failed to induce any change in PARP-1 expression and activation, DNA single‑strand breaks or plasma membrane integrity. Pre-exposure to hypoxia markedly increased the sensitivity of the cells to subsequent oxidative stress-induced DNA damage. Hydrogen peroxide (H2O2) induced a concentration-dependent increase in DNA breakage, PARP activation, depletion of intracellular ATP, inhibition of mitochondrial activity and two distinct parameters that quantify the breakdown of plasma membrane integrity (propidium iodide uptake or lactate dehydrogenase release). PARP-1 activation played a significant role in the H2O2-induced cell death response because PARP activation, depletion of intracellular ATP, inhibition of mitochondrial activity, and the breakdown of plasma membrane integrity were attenuated in cells with permanently silenced PARP-1. Based on measurement of the endogenous antioxidant GSH, we hypothesized that the mechanism of hypoxia-mediated enhancement of H2O2 involves depletion of the GSH during the hypoxic period, which renders the cells more sensitive to a subsequent DNA single‑strand break elicited by H2O2. DNA strand breakage then activates PARP-1, leading to the inhibition of mitochondrial function, depletion of ATP and cell necrosis. PARP-1 deficiency protects against the cytotoxicity, to a lesser degree, by protecting against GSH depletion during the hypoxic period, and, to a larger degree, by maintaining mitochondrial function and preserving intracellular ATP levels during the subsequent oxidative stress period.
MeSH term(s)	Cell Death ; Cell Hypoxia ; Cell Line, Tumor ; Cell Transformation, Neoplastic/metabolism ; DNA Damage ; Glutathione/metabolism ; Humans ; Hydrogen Peroxide/metabolism ; Hypoxia/metabolism ; Oxidative Stress ; Poly (ADP-Ribose) Polymerase-1 ; Poly(ADP-ribose) Polymerases/metabolism
Chemical Substances	Hydrogen Peroxide (BBX060AN9V) ; PARP1 protein, human (EC 2.4.2.30) ; Poly (ADP-Ribose) Polymerase-1 (EC 2.4.2.30) ; Poly(ADP-ribose) Polymerases (EC 2.4.2.30) ; Glutathione (GAN16C9B8O)
Language	English
Publishing date	2013-05-29
Publishing country	Greece
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1444428-8
ISSN	1791-244X ; 1107-3756
ISSN (online)	1791-244X
ISSN	1107-3756
DOI	10.3892/ijmm.2013.1397
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Article ; Online: Cannabinoid-2 receptor activation ameliorates hepatorenal syndrome.

Trojnar, Eszter / Erdelyi, Katalin / Matyas, Csaba / Zhao, Suxian / Paloczi, Janos / Mukhopadhyay, Partha / Varga, Zoltan V / Hasko, Gyorgy / Pacher, Pal

Free radical biology & medicine

2019 Volume 152, Page(s) 540–550

Abstract: Study rationale: Hepatorenal syndrome (HRS) is a life-threatening complication of end-stage liver disease characterized by the rapid decline of kidney function. Herein, we explored the therapeutic potential of targeting the cannabinoid-2 receptor (CB: ...

Abstract	Study rationale: Hepatorenal syndrome (HRS) is a life-threatening complication of end-stage liver disease characterized by the rapid decline of kidney function. Herein, we explored the therapeutic potential of targeting the cannabinoid-2 receptor (CB Methods: Gene expression analysis, histological evaluation, determination of serum levels of renal injury-biomarkers were used to characterize the BDL-induced organ injury; laser speckle analysis to measure microcirculation in the kidneys. Key results: We found that liver injury triggered marked inflammation and oxidative stress in the kidneys of BDL-operated mice. We detected pronounced histopathological alterations with tubular injury paralleled with increased inflammation, oxidative/nitrative stress and fibrotic remodeling both in hepatic and renal tissues as well as endothelial activation and markedly impaired renal microcirculation. This was accompanied by increased CB Conclusions: Our results suggest that oxidative stress, inflammation and microvascular dysfunction are key events in the pathogenesis of BDL-associated renal failure. Furthermore, we demonstrate that targeting the CB
MeSH term(s)	Animals ; Bile Ducts/surgery ; Cannabinoids ; Disease Models, Animal ; Hepatorenal Syndrome/drug therapy ; Hepatorenal Syndrome/etiology ; Hepatorenal Syndrome/metabolism ; Liver/metabolism ; Mice ; Microcirculation ; Oxidative Stress ; Receptors, Cannabinoid/metabolism
Chemical Substances	Cannabinoids ; Receptors, Cannabinoid
Language	English
Publishing date	2019-11-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
ZDB-ID	807032-5
ISSN	1873-4596 ; 0891-5849
ISSN (online)	1873-4596
ISSN	0891-5849
DOI	10.1016/j.freeradbiomed.2019.11.027
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Zs.A 2109: Show issues

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Article ; Online: Interplay of Liver-Heart Inflammatory Axis and Cannabinoid 2 Receptor Signaling in an Experimental Model of Hepatic Cardiomyopathy.

Matyas, Csaba / Erdelyi, Katalin / Trojnar, Eszter / Zhao, Suxian / Varga, Zoltan V / Paloczi, Janos / Mukhopadhyay, Partha / Nemeth, Balazs T / Haskó, György / Cinar, Resat / Rodrigues, Robim M / Ait Ahmed, Yeni / Gao, Bin / Pacher, Pal

Hepatology (Baltimore, Md.)

2020 Volume 71, Issue 4, Page(s) 1391–1407

Abstract: Background and aims: Hepatic cardiomyopathy, a special type of heart failure, develops in up to 50% of patients with cirrhosis and is a major determinant of survival. However, there is no reliable model of hepatic cardiomyopathy in mice. We aimed to ... ...

Abstract	Background and aims: Hepatic cardiomyopathy, a special type of heart failure, develops in up to 50% of patients with cirrhosis and is a major determinant of survival. However, there is no reliable model of hepatic cardiomyopathy in mice. We aimed to characterize the detailed hemodynamics of mice with bile duct ligation (BDL)-induced liver fibrosis, by monitoring echocardiography and intracardiac pressure-volume relationships and myocardial structural alterations. Treatment of mice with a selective cannabinoid-2 receptor (CB Approach and results: BDL induced massive inflammation (increased leukocyte infiltration, inflammatory cytokines, and chemokines), oxidative stress, microvascular dysfunction, and fibrosis in the liver. These pathological changes were accompanied by impaired diastolic, systolic, and macrovascular functions; cardiac inflammation (increased macrophage inflammatory protein 1, interleukin-1, P-selectin, cluster of differentiation 45-positive cells); and oxidative stress (increased malondialdehyde, 3-nitrotyrosine, and nicotinamide adenine dinucleotide phosphate oxidases). CB Conclusions: We propose BDL-induced cardiomyopathy in mice as a model for hepatic/cirrhotic cardiomyopathy. This cardiomyopathy, similar to cirrhotic cardiomyopathy in humans, is characterized by systemic hypotension and impaired macrovascular and microvascular function accompanied by both systolic and diastolic dysfunction. Our results indicate that the liver-heart inflammatory axis has a pivotal pathophysiological role in the development of hepatic cardiomyopathy. Thus, controlling liver and/or myocardial inflammation (e.g., with selective CB
MeSH term(s)	Animals ; Cardiomyopathies/etiology ; Cardiomyopathies/pathology ; Disease Models, Animal ; Heart Failure/etiology ; Heart Failure/pathology ; Hepatitis/metabolism ; Hepatitis/pathology ; Inflammation/metabolism ; Inflammation/pathology ; Liver ; Liver Cirrhosis/complications ; Liver Cirrhosis/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Myocarditis/metabolism ; Myocarditis/pathology ; Myocardium/metabolism ; Myocardium/pathology ; Receptor, Cannabinoid, CB2/agonists ; Receptor, Cannabinoid, CB2/metabolism ; Signal Transduction
Chemical Substances	Cnr2 protein, mouse ; Receptor, Cannabinoid, CB2
Language	English
Publishing date	2020-01-24
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural
ZDB-ID	604603-4
ISSN	1527-3350 ; 0270-9139
ISSN (online)	1527-3350
ISSN	0270-9139
DOI	10.1002/hep.30916
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Zs.A 1660: Show issues

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Article ; Online: Reprogrammed transsulfuration promotes basal-like breast tumor progression via realigning cellular cysteine persulfidation.

Erdélyi, Katalin / Ditrói, Tamás / Johansson, Henrik J / Czikora, Ágnes / Balog, Noémi / Silwal-Pandit, Laxmi / Ida, Tomoaki / Olasz, Judit / Hajdú, Dorottya / Mátrai, Zoltán / Csuka, Orsolya / Uchida, Koji / Tóvári, József / Engebraten, Olav / Akaike, Takaaki / Børresen Dale, Anne-Lise / Kásler, Miklós / Lehtiö, Janne / Nagy, Péter

Proceedings of the National Academy of Sciences of the United States of America

2021 Volume 118, Issue 45

Abstract: Basal-like breast cancer (BLBC) is the most aggressive subtype of breast tumors with poor prognosis and limited molecular-targeted therapy options. We show that BLBC cells have a high Cys demand and reprogrammed Cys metabolism. Patient-derived BLBC ... ...

Abstract	Basal-like breast cancer (BLBC) is the most aggressive subtype of breast tumors with poor prognosis and limited molecular-targeted therapy options. We show that BLBC cells have a high Cys demand and reprogrammed Cys metabolism. Patient-derived BLBC tumors from four different cohorts exhibited elevated expression of the transsulfuration enzyme cystathione β-synthetase (CBS). CBS silencing (shCBS) made BLBC cells less invasive, proliferate slower, more vulnerable to oxidative stress and cystine (CySSCy) deprivation, prone to ferroptosis, and less responsive to HIF1-α activation under hypoxia. shCBS xenograft tumors grew slower than controls and exhibited impaired angiogenesis and larger necrotic areas. Sulfur metabolite profiling suggested that realigned sulfide/persulfide-inducing functions of CBS are important in BLBC tumor progression. Supporting this, the exclusion of serine, a substrate of CBS for producing Cys but not for producing sulfide/persulfide, did not exacerbate CySSCy deprivation-induced ferroptosis in shCBS BLBC cells. Impaired Tyr phosphorylation was detected in shCBS cells and xenografts, likely due to persulfidation-inhibited phosphatase functions. Overexpression of cystathione γ-lyase (CSE), which can also contribute to cellular sulfide/persulfide production, compensated for the loss of CBS activities, and treatment of shCBS xenografts with a CSE inhibitor further blocked tumor growth. Glutathione and protein-Cys levels were not diminished in shCBS cells or xenografts, but levels of Cys persulfidation and the persulfide-catabolizing enzyme ETHE1 were suppressed. Finally, expression of enzymes of the oxidizing Cys catabolism pathway was diminished, but expression of the persulfide-producing CARS2 was elevated in human BLBC tumors. Hence, the persulfide-producing pathways are major targetable determinants of BLBC pathology that could be therapeutically exploited.
MeSH term(s)	Animals ; Cohort Studies ; Cystathionine beta-Synthase/metabolism ; Cysteine/metabolism ; Disease Progression ; Female ; Ferroptosis ; Humans ; Mice, SCID ; Neovascularization, Pathologic ; Oxidative Stress ; Sulfides/metabolism ; Triple Negative Breast Neoplasms/enzymology ; Mice
Chemical Substances	Sulfides ; persulfides ; Cystathionine beta-Synthase (EC 4.2.1.22) ; Cysteine (K848JZ4886)
Language	English
Publishing date	2021-10-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2100050118
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Article ; Online: Intramitochondrial hydrogen sulfide production by 3-mercaptopyruvate sulfurtransferase maintains mitochondrial electron flow and supports cellular bioenergetics.

Módis, Katalin / Coletta, Ciro / Erdélyi, Katalin / Papapetropoulos, Andreas / Szabo, Csaba

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

2013 Volume 27, Issue 2, Page(s) 601–611

Abstract: It is well established that exposure of mammalian cells to hydrogen sulfide (H(2)S) suppresses mitochondrial function by inhibiting cytochrome-c oxidase (CcOX; complex IV). However, recent experimental data show that administration of H(2)S to mammalian ... ...

Abstract	It is well established that exposure of mammalian cells to hydrogen sulfide (H(2)S) suppresses mitochondrial function by inhibiting cytochrome-c oxidase (CcOX; complex IV). However, recent experimental data show that administration of H(2)S to mammalian cells can serve as an electron donor and inorganic source of energy. The aim of our study was to investigate the role of endogenously produced H(2)S in the regulation of mitochondrial electron transport and oxidative phosphorylation in isolated liver mitochondria and in the cultured murine hepatoma cell line Hepa1c1c7. Low concentrations of H(2)S (0.1-1 μM) elicited a significant increase in mitochondrial function, while higher concentrations of H(2)S (3-30 μM) were inhibitory. The positive bioenergetic effect of H(2)S required a basal activity of the Krebs cycle and was most pronounced at intermediate concentrations of succinate. 3-mercaptopyruvate (3-MP), the substrate of the mitochondrial enzyme 3-mercaptopyruvate sulfurtransferase (3-MST) stimulated mitochondrial H(2)S production and enhanced mitochondrial electron transport and cellular bioenergetics at low concentrations (10-100 nM), while at higher concentrations, it inhibited cellular bioenergetics. SiRNA silencing of 3-MST reduced basal bioenergetic parameters and prevented the stimulating effect of 3-MP on mitochondrial bioenergetics. Silencing of sulfide quinone oxidoreductase (SQR) also reduced basal and 3-MP-stimulated bioenergetic parameters. We conclude that an endogenous intramitochondrial H(2)S-producing pathway, governed by 3-MST, complements and balances the bioenergetic role of Krebs cycle-derived electron donors. This pathway may serve a physiological role in the maintenance of mitochondrial electron transport and cellular bioenergetics.
MeSH term(s)	Animals ; Base Sequence ; Cell Line ; Citric Acid Cycle ; Cysteine/analogs & derivatives ; Cysteine/metabolism ; Electron Transport ; Energy Metabolism ; Hydrogen Sulfide/metabolism ; Male ; Mice ; Mitochondria, Liver/metabolism ; Models, Biological ; Oxidative Phosphorylation ; Quinone Reductases/antagonists & inhibitors ; Quinone Reductases/genetics ; Quinone Reductases/metabolism ; RNA, Small Interfering/genetics ; Rats ; Rats, Sprague-Dawley ; Sulfurtransferases/antagonists & inhibitors ; Sulfurtransferases/genetics ; Sulfurtransferases/metabolism
Chemical Substances	RNA, Small Interfering ; 3-mercaptopyruvic acid (5Z1F5OW4YB) ; Quinone Reductases (EC 1.6.99.-) ; sulfide quinone reductase (EC 1.8.5.-) ; Sulfurtransferases (EC 2.8.1.-) ; 3-mercaptopyruvate sulphurtransferase (EC 2.8.1.2) ; Cysteine (K848JZ4886) ; Hydrogen Sulfide (YY9FVM7NSN)
Language	English
Publishing date	2013-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639186-2
ISSN	1530-6860 ; 0892-6638
ISSN (online)	1530-6860
ISSN	0892-6638
DOI	10.1096/fj.12-216507
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Zs.A 2266: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Design, Synthesis, and Biological Evaluation of Novel, Non-Brain-Penetrant, Hybrid Cannabinoid CB

Iyer, Malliga R / Cinar, Resat / Katz, Alexis / Gao, Michael / Erdelyi, Katalin / Jourdan, Tony / Coffey, Nathan J / Pacher, Pal / Kunos, George

Journal of medicinal chemistry

2017 Volume 60, Issue 3, Page(s) 1126–1141

Abstract: We report the design, synthesis, and structure-activity relationships of novel dual-target compounds with antagonist/inverse agonist activity at cannabinoid receptor type 1 ( ... ...

Abstract	We report the design, synthesis, and structure-activity relationships of novel dual-target compounds with antagonist/inverse agonist activity at cannabinoid receptor type 1 (CB
MeSH term(s)	Animals ; Brain/metabolism ; CHO Cells ; Cricetinae ; Cricetulus ; Drug Design ; Enzyme Inhibitors/metabolism ; Humans ; Liver Cirrhosis/drug therapy ; Mice ; Nitric Oxide Synthase Type II/antagonists & inhibitors ; Receptor, Cannabinoid, CB1/antagonists & inhibitors ; Structure-Activity Relationship
Chemical Substances	Enzyme Inhibitors ; Receptor, Cannabinoid, CB1 ; Nitric Oxide Synthase Type II (EC 1.14.13.39)
Language	English
Publishing date	2017-01-27
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural
ZDB-ID	218133-2
ISSN	1520-4804 ; 0022-2623
ISSN (online)	1520-4804
ISSN	0022-2623
DOI	10.1021/acs.jmedchem.6b01504
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Article: Cellular bioenergetics is regulated by PARP1 under resting conditions and during oxidative stress

Módis, Katalin / Gerő, Domokos / Erdélyi, Katalin / Szoleczky, Petra / DeWitt, Douglas / Szabo, Csaba

Biochemical Pharmacology. 2012 Mar. 1, v. 83, no. 5

2012

Abstract: PURPOSE: The goal of the current studies was to elucidate the role of the principal poly(ADP-ribose)polymerase isoform, PARP1 in the regulation of cellular energetics in endothelial cells under resting conditions and during oxidative stress. METHODS: We ... ...

Abstract	PURPOSE: The goal of the current studies was to elucidate the role of the principal poly(ADP-ribose)polymerase isoform, PARP1 in the regulation of cellular energetics in endothelial cells under resting conditions and during oxidative stress. METHODS: We utilized bEnd.3 endothelial cells and A549 human transformed epithelial cells. PARP1 was inhibited either by pharmacological inhibitors or by siRNA silencing. The Seahorse XF24 Extracellular Flux Analyzer was used to measure indices of mitochondrial respiration (oxygen consumption rate) and of glycolysis (extracellular acidification rate). Cell viability, cellular and mitochondrial NAD⁺ levels and mitochondrial biogenesis were also measured. RESULTS: Silencing of PARP1 increased basal cellular parameters of oxidative phosphorylation, providing direct evidence that PARP1 is a regulator of mitochondrial function in resting cells. Pharmacological inhibitors of PARP1 and siRNA silencing of PARP1 protected against the development of mitochondrial dysfunction and elevated the respiratory reserve capacity in endothelial and epithelial cells exposed to oxidative stress. The observed effects were unrelated to an effect on mitochondrial biogenesis. Isolated mitochondria of A549 human transformed epithelial cells exhibited an improved resting bioenergetic status after stable lentiviral silencing of PARP1; these effects were associated with elevated resting mitochondrial NAD⁺ levels in PARP1 silenced cells. CONCLUSIONS: PARP1 is a regulator of basal cellular energetics in resting endothelial and epithelial cells. Furthermore, endothelial cells respond with a decrease in their mitochondrial reserve capacity during low-level oxidative stress, an effect, which is attenuated by PARP1 inhibition. While PARP1 is a regulator of oxidative phosphorylation in resting and oxidatively stressed cells, it only exerts a minor effect on glycolysis.
Keywords	acidification ; biogenesis ; cell viability ; endothelial cells ; epithelial cells ; glycolysis ; humans ; mitochondria ; oxidative phosphorylation ; oxidative stress ; oxygen consumption ; pharmacology
Language	English
Dates of publication	2012-0301
Size	p. 633-643.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	208787-x
ISSN	1873-2968 ; 0006-2952
ISSN (online)	1873-2968
ISSN	0006-2952
DOI	10.1016/j.bcp.2011.12.014
Database	NAL-Catalogue (AGRICOLA)

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