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Article ; Online: Metabolic plasticity in blast crisis-chronic myeloid leukaemia cells under hypoxia reduces the cytotoxic potency of drugs targeting mitochondria.

Salaverry, Luciana S / Lombardo, Tomás / Cabral-Lorenzo, María C / Gil-Folgar, Martin L / Rey-Roldán, Estela B / Kornblihtt, Laura I / Blanco, Guillermo A

Discover. Oncology

2022 Volume 13, Issue 1, Page(s) 60

Abstract: Metabolic reprogramming (MR) influences progression of chronic myeloid leukaemia (CML) to blast crisis (BC), but metabolic programs may change transiently in a second dimension (metabolic plasticity, MP), driven by environments as hypoxia, affecting ... ...

Abstract	Metabolic reprogramming (MR) influences progression of chronic myeloid leukaemia (CML) to blast crisis (BC), but metabolic programs may change transiently in a second dimension (metabolic plasticity, MP), driven by environments as hypoxia, affecting cytotoxic potency (CPot) of drugs targeting mitochondria or mitochondria-related cell stress responses (MRCSR) such as mitophagy and mitochondrial biogenesis. We assessed mitochondrial membrane potential (MMP), mitochondrial mass (MM), apoptosis, glucose uptake (GU), and CPot of arsenic trioxide (ATO), CCCP, valproic acid (VPA), vincristine (VCR), Mdivi1, and dichloroacetic acid (DCA) in CML BC cells K562 (BC-K562) under hypoxia through flow cytometry, and gene expression from GEO database. About 60% of untreated cells were killed after 72 h under hypoxia, but paradoxically, all drugs but ATO rescued cells and increased survival rates to almost 90%. Blocking mitophagy either with VCR or Mdivi1, or increasing mitochondrial biogenesis with VPA enhanced cell-survival with increased MM. DCA increased MM and rescued cells in spite of its role in activating pyruvate dehydrogenase and Krebs cycle. Cells rescued by DCA, VPA and CCCP showed decreased GU. ATO showed equal CPot in hypoxia and normoxia. MP was evidenced by differential expression of genes (DEG) under hypoxia related to Krebs cycle, lipid synthesis, cholesterol homeostasis, mitophagy, and mitochondrial biogenesis (GSE144527). A 25-gene MP-signature of BC-K562 cells under hypoxia identified BC cases among 113 transcriptomes from CML patients (GSE4170). We concluded that hypoxic environment drove a MP change evidenced by DEG that was reflected in a paradoxical pro-survival, instead of cytotoxic, effect of drugs targeting mitochondria and MRCSR.
Language	English
Publishing date	2022-07-08
Publishing country	United States
Document type	Journal Article
ISSN	2730-6011
ISSN (online)	2730-6011
DOI	10.1007/s12672-022-00524-y
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Article ; Online: Losartan impairs HTR-8/SVneo trophoblast migration through inhibition of angiotensin II-induced pro-inflammatory profile in human endometrial stromal cells.

Macchi, Rosario / Sotelo, Agustina D / Parrado, Andrea C / Salaverry, Luciana S / Blanco, Guillermo A / Castro, Marisa S / Rey-Roldán, Estela B / Canellada, Andrea M

Toxicology and applied pharmacology

2023 Volume 461, Page(s) 116383

Abstract: A deep interaction between the endometrium and the invading trophoblast occurs during implantation in humans, with the acquisition of uterine receptivity to the invading embryo promoted by an elevation of pro-inflammatory cytokines in the endometrium, ... ...

Abstract	A deep interaction between the endometrium and the invading trophoblast occurs during implantation in humans, with the acquisition of uterine receptivity to the invading embryo promoted by an elevation of pro-inflammatory cytokines in the endometrium, and the invasiveness of decidualizing endometrial stromal cells, augmented by trophoblast-derived signals. Considering that usage of angiotensin II type 1 (AT1) receptor blockers, among other renin-angiotensin system (RAS) antagonists, is associated with adverse pregnancy outcomes, here we aim to analyse the involvement of AT1 receptor in the reciprocal dialogue occurring between endometrial stroma and trophoblast cells. In human endometrial stromal cells (T-HESC) pre-incubated with a decidualization cocktail, angiotensin (Ang) II increased protein expression of prolactin and FOXO1, markers of endometrial decidualization, while promoting nuclear translocation of FOXO1. In addition, Ang II treatment increased CXCL8, and matrix metalloprotease (MMP)-2 levels in T-HESC. Incubation with the AT1 receptor blocker losartan or with an NFAT signalling inhibitor, decreased Ang II-induced secretion of prolactin, CXCL8, and MMP-2 in T-HESC. In a wound healing assay, conditioned medium (CM) obtained from Ang II-treated T-HESC, but not CM from losartan-pre-incubated T-HESC, increased migration of HTR-8/SVneo trophoblasts, effect that was inhibited in the presence of a CXCL8-neutralizing antibody. An increased secretion of CXCL8 and MMP-2 was observed after treatment of T-HESC with CM obtained from HTR-8/SVneo cells, which was not observed in T-HESC pre-incubated with losartan or with the NFAT inhibitor. This study evidenced a reciprocal RAS-coded messaging between trophoblast and ESC which is affected by the AT1 receptor blocker losartan.
MeSH term(s)	Pregnancy ; Female ; Humans ; Trophoblasts/metabolism ; Losartan/pharmacology ; Angiotensin II/toxicity ; Receptor, Angiotensin, Type 1/metabolism ; Matrix Metalloproteinase 2/metabolism ; Prolactin/metabolism ; Endometrium/metabolism ; Stromal Cells/metabolism
Chemical Substances	Losartan (JMS50MPO89) ; Angiotensin II (11128-99-7) ; Receptor, Angiotensin, Type 1 ; Matrix Metalloproteinase 2 (EC 3.4.24.24) ; Prolactin (9002-62-4)
Language	English
Publishing date	2023-01-20
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	204477-8
ISSN	1096-0333 ; 0041-008X
ISSN (online)	1096-0333
ISSN	0041-008X
DOI	10.1016/j.taap.2023.116383
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Article ; Online: Clot Formation in the Sipunculid Worm Themiste petricola: A Haemostatic and Immune Cellular Response.

Lombardo, Tomás / Blanco, Guillermo A

International journal of cell biology

2012 Volume 2012, Page(s) 280675

Abstract: Clot formation in the sipunculid Themiste petricola, a coelomate nonsegmented marine worm without a circulatory system, is a cellular response that creates a haemostatic mass upon activation with sea water. The mass with sealing properties is brought ... ...

Abstract	Clot formation in the sipunculid Themiste petricola, a coelomate nonsegmented marine worm without a circulatory system, is a cellular response that creates a haemostatic mass upon activation with sea water. The mass with sealing properties is brought about by homotypic aggregation of granular leukocytes present in the coelomic fluid that undergo a rapid process of fusion and cell death forming a homogenous clot or mass. The clot structure appears to be stabilized by abundant F-actin that creates a fibrous scaffold retaining cell-derived components. Since preservation of fluid within the coelom is vital for the worm, clotting contributes to rapidly seal the body wall and entrap pathogens upon injury, creating a matrix where wound healing can take place in a second stage. During formation of the clot, microbes or small particles are entrapped. Phagocytosis of self and non-self particles shed from the clot occurs at the clot neighbourhood, demonstrating that clotting is the initial phase of a well-orchestrated dual haemostatic and immune cellular response.
Language	English
Publishing date	2012-03-25
Publishing country	United States
Document type	Journal Article
ZDB-ID	2536742-0
ISSN	1687-8884 ; 1687-8884
ISSN (online)	1687-8884
ISSN	1687-8884
DOI	10.1155/2012/280675
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Article ; Online: Regulated Cell Death of Lymphoma Cells after Graded Mitochondrial Damage is Differentially Affected by Drugs Targeting Cell Stress Responses.

Lombardo, Tomás / Folgar, Martín Gil / Salaverry, Luciana / Rey-Roldán, Estela / Alvarez, Elida M / Carreras, María C / Kornblihtt, Laura / Blanco, Guillermo A

Basic & clinical pharmacology & toxicology

2018 Volume 122, Issue 5, Page(s) 489–500

Abstract: Collapse of the mitochondrial membrane potential (MMP) is often considered the initiation of regulated cell death (RCD). Carbonyl cyanide 3-chlorophenylhydrazone (CCCP) is an uncoupler of the electron transport chain (ETC) that facilitates the ... ...

Abstract	Collapse of the mitochondrial membrane potential (MMP) is often considered the initiation of regulated cell death (RCD). Carbonyl cyanide 3-chlorophenylhydrazone (CCCP) is an uncoupler of the electron transport chain (ETC) that facilitates the translocation of protons into the mitochondrial matrix leading to the collapse of the MMP. Several cell stress responses such as mitophagy, mitochondrial biogenesis and the ubiquitin proteasome system may differentially contribute to restrain the initiation of RCD depending on the extent of mitochondrial damage. We induced graded mitochondrial damage after collapse of MMP with the mitochondrial uncoupler CCCP in Burkitt's lymphoma cells, and we evaluated the effect of several drugs targeting cell stress responses over RCD at 72 hr, using a multiparametric flow cytometry approach. CCCP caused collapse of MMP after 30 min., massive mitochondrial fission, oxidative stress and increased mitophagy within the 5-15 μM low-dose range (LDR) of CCCP. Within the 20-50 μM high-dose range (HDR), CCCP caused lysosomal destabilization and rupture, thus precluding mitophagy and autophagy. Cell death after 72 hr was below 20%, with increased mitochondrial mass (MM). The inhibitors of mitophagy 3-(2,4-dichloro-5-methoxyphenyl)-2,3-dihydro-2-thioxo-4(1H)-quinazolinone (Mdivi-1) and vincristine (VCR) increased cell death from CCCP within the LDR, while valproic acid (an inducer of mitochondrial biogenesis) also increased MM and cell death within the LDR. The proteasome inhibitor, MG132, increased cell death only in the HDR. Doxycycline, an antibiotic that disrupts mitochondrial biogenesis, had no effect on cell survival, while iodoacetamide, an inhibitor of glycolysis, increased cell death at the HDR. We conclude that mitophagy influenced RCD of lymphoma cells after MMP collapse by CCCP only within the LDR, while proteasome activity and glycolysis contributed to survival in the HDR under extensive mitochondria and lysosome damage.
MeSH term(s)	Autophagosomes/drug effects ; Autophagosomes/metabolism ; Autophagosomes/pathology ; Autophagy/drug effects ; Burkitt Lymphoma/drug therapy ; Burkitt Lymphoma/metabolism ; Burkitt Lymphoma/pathology ; Carbonyl Cyanide m-Chlorophenyl Hydrazone/pharmacology ; Cell Line, Tumor ; Cell Survival/drug effects ; Dose-Response Relationship, Drug ; Humans ; Iodoacetamide/pharmacology ; Leupeptins/pharmacology ; Lysosomes/drug effects ; Lysosomes/metabolism ; Lysosomes/pathology ; Membrane Potential, Mitochondrial/drug effects ; Mitochondria/drug effects ; Mitochondria/metabolism ; Mitochondria/pathology ; Mitochondrial Degradation/drug effects ; Mitochondrial Dynamics/drug effects ; Oxidative Stress/drug effects ; Proteasome Endopeptidase Complex/drug effects ; Proteasome Endopeptidase Complex/metabolism ; Proteasome Inhibitors/pharmacology ; Quinazolinones/pharmacology ; Reactive Oxygen Species/metabolism ; Time Factors ; Uncoupling Agents/pharmacology ; Unfolded Protein Response/drug effects ; Vincristine/pharmacology
Chemical Substances	3-(2,4-dichloro-5-methoxyphenyl)-2-sulfanyl-4(3H)-quinazolinone ; Leupeptins ; Proteasome Inhibitors ; Quinazolinones ; Reactive Oxygen Species ; Uncoupling Agents ; Carbonyl Cyanide m-Chlorophenyl Hydrazone (555-60-2) ; Vincristine (5J49Q6B70F) ; Proteasome Endopeptidase Complex (EC 3.4.25.1) ; benzyloxycarbonylleucyl-leucyl-leucine aldehyde (RF1P63GW3K) ; Iodoacetamide (ZRH8M27S79)
Language	English
Publishing date	2018-01-03
Publishing country	England
Document type	Journal Article
ZDB-ID	2134679-3
ISSN	1742-7843 ; 1742-7835
ISSN (online)	1742-7843
ISSN	1742-7835
DOI	10.1111/bcpt.12945
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Article ; Online: A drug potency signature links progression of chronic lymphocytic leukemia to mitochondria-related stress responses and metabolic reprogramming under hypoxia.

Kornblihtt, Laura I / Cabral Lorenzo, María C / Gil Folgar, Martin L / Minissale, Clelia J / Malusardi, Cecilia / Rojas, Francisca / Lombardo, Tomás / Blanco, Guillermo A

Toxicology and applied pharmacology

2020 Volume 398, Page(s) 115016

Abstract: Chronic lymphocytic leukemia (CLL) cells change their metabolic program between normoxia and hypoxia, possibly affecting cytotoxic drug potency by altering mitochondria-related cell stress responses (MRCSR) including mitophagy, mitochondrial biogenesis, ... ...

Abstract	Chronic lymphocytic leukemia (CLL) cells change their metabolic program between normoxia and hypoxia, possibly affecting cytotoxic drug potency by altering mitochondria-related cell stress responses (MRCSR) including mitophagy, mitochondrial biogenesis, and mitochondrial proteostasis. We evaluated in CLL cells from nine patients, the single and multiple-combined drug potency of arsenic trioxide (ATO), valproic acid (VPA), vincristine (VCR) and MG132 as four pharmacological sensors influencing mitochondrial apoptosis, mitochondrial biogenesis, mitophagy, and mitochondrial proteostasis respectively, under normoxia and hypoxia to force hypoxia-induced metabolic reprogramming (HMR). Untreated cells from all patients remained viable under O
MeSH term(s)	Aged ; Aged, 80 and over ; Antineoplastic Agents/pharmacology ; Apoptosis/drug effects ; Cell Line, Tumor ; Cell Survival/drug effects ; Disease Progression ; Female ; Humans ; Hypoxia/drug therapy ; Hypoxia/metabolism ; Hypoxia/pathology ; Leukemia, Lymphocytic, Chronic, B-Cell/drug therapy ; Leukemia, Lymphocytic, Chronic, B-Cell/metabolism ; Leukemia, Lymphocytic, Chronic, B-Cell/pathology ; Male ; Middle Aged ; Mitochondria/drug effects ; Mitochondria/metabolism ; Mitochondria/pathology ; Signal Transduction/drug effects
Chemical Substances	Antineoplastic Agents
Language	English
Publishing date	2020-04-20
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	204477-8
ISSN	1096-0333 ; 0041-008X
ISSN (online)	1096-0333
ISSN	0041-008X
DOI	10.1016/j.taap.2020.115016
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Article: Sulfenylation of nitroalkanes and hydroxyaryls

Blanco, Guillermo A / Baumgartner, Maria T

Tetrahedron letters. 2011 Dec. 28, v. 52, no. 52

2011

Abstract: The sulfenylation of nitroalkanes and hydroxyaryls in DMSO using aryl disulfides as sulfenylating reagents was studied. The corresponding arylthionitroalkanes and arylthiohydroxyaryls were obtained in moderate to good yields in very mild conditions, thus ...

Abstract	The sulfenylation of nitroalkanes and hydroxyaryls in DMSO using aryl disulfides as sulfenylating reagents was studied. The corresponding arylthionitroalkanes and arylthiohydroxyaryls were obtained in moderate to good yields in very mild conditions, thus improving the reported procedures for the synthesis of these compounds.
Keywords	chemical reactions ; chemical structure ; dimethyl sulfoxide
Language	English
Dates of publication	2011-1228
Size	p. 7061-7063.
Publishing place	Elsevier Ltd
Document type	Article
ZDB-ID	204287-3
ISSN	1873-3581 ; 0040-4039
ISSN (online)	1873-3581
ISSN	0040-4039
DOI	10.1016/j.tetlet.2011.10.053
Database	NAL-Catalogue (AGRICOLA)

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Article: Immune systems, geographic information systems (GIS), environment and health impacts.

Blanco, Guillermo A / Cooper, Edwin L

Journal of toxicology and environmental health. Part B, Critical reviews

2004 Volume 7, Issue 6, Page(s) 465–480

Abstract: Exposure to dioxins, polychlorinated biphenyls (PCBs), and polycyclic aromatic hydrocarbons (PAHs) has been related to alterations in cellular and humoral immune responses in both adaptive and innate immune systems of most animal species. These compounds ...

Abstract	Exposure to dioxins, polychlorinated biphenyls (PCBs), and polycyclic aromatic hydrocarbons (PAHs) has been related to alterations in cellular and humoral immune responses in both adaptive and innate immune systems of most animal species. These compounds share a common signaling mechanism to exert their effects on cells of the immune system, which includes the aryl-hydrocarbon receptor (AhR) and the AhR nuclear translocator (ARN). Recently, the interference of AhR-ARNT with the nuclear factor (NF)-kappaB signaling pathway has been proposed as a critical event in the adverse effects on the immune system. Studies on the effects of these AhR-ARNT-related toxicants on the immune system of higher and lower phylum animals and knowledge of intracellular mechanisms of toxicity may contribute to development of biomarkers of ecotoxicant exposure and effects. Biomarkers of this kind allow sampling over extended geographic areas, in several sentinel species, including wildlife animals, and facilitate the building of risk models and risk maps of environmentally induced diseases. On the basis of location, biomarker sampled data obtained through evaluation of ecotoxicant exposure and effects on the immune system in sentinel species can be further integrated and analyzed together with other sources of environmental geographic information, or human population health data, by means of geographic information systems (GIS). The spatial analysis capability of GIS can help to evaluate the complex relationships of overlaid information and to identify areas with high risk indices or "hot spots." This integrative approach can be useful in studies contributing to support environmental and health-related policies and regulations.
MeSH term(s)	Animals ; Animals, Wild ; Dioxins/poisoning ; Environmental Exposure ; Environmental Health ; Environmental Monitoring/methods ; Environmental Pollutants/poisoning ; Geographic Information Systems ; Humans ; Immune System/drug effects ; Immune System/physiology ; Polychlorinated Biphenyls/poisoning ; Polycyclic Aromatic Hydrocarbons/poisoning ; Risk Assessment
Chemical Substances	Dioxins ; Environmental Pollutants ; Polycyclic Aromatic Hydrocarbons ; Polychlorinated Biphenyls (DFC2HB4I0K)
Language	English
Publishing date	2004-11
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1415246-0
ISSN	1521-6950 ; 1093-7404
ISSN (online)	1521-6950
ISSN	1093-7404
DOI	10.1080/10937400490512375
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Article ; Online: Synergism of arsenic trioxide and MG132 in Raji cells attained by targeting BNIP3, autophagy, and mitochondria with low doses of valproic acid and vincristine.

Cavaliere, Victoria / Lombardo, Tomás / Costantino, Susana N / Kornblihtt, Laura / Alvarez, Elida M / Blanco, Guillermo A

European journal of cancer (Oxford, England : 1990)

2014 Volume 50, Issue 18, Page(s) 3243–3261

Abstract: We previously demonstrated that arsenic trioxide (ATO) and proteasome inhibitor MG132 synergistically induced cell death in promonocytic leukaemia cell line U937 but were antagonistic in Burkitt's lymphoma cell line Raji. Here we explore the role of ... ...

Abstract	We previously demonstrated that arsenic trioxide (ATO) and proteasome inhibitor MG132 synergistically induced cell death in promonocytic leukaemia cell line U937 but were antagonistic in Burkitt's lymphoma cell line Raji. Here we explore the role of autophagy, expression of BNIP3, and mitochondrial mass, in determining whether ATO and MG132 interaction can be shifted from antagonism to synergism in Raji cells. Treatment with ATO+MG132 increased the percentage of cells with collapsed mitochondrial membrane potential (MMP) in U937 cells, but had no effect in Raji cells. Mitochondria were found in cytoplasmic marginal location in U937 cells but at perinuclear location in Raji cells. ATO+MG132 increased mitochondrial mass in U937 cells but decreased it in Raji cells, while autophagy was increased in both cell lines. BNIP3 was expressed in U937 cells at cytoplasmic marginal locations and was hardly detected in Raji cells. Histone deacetylase (HDAC) inhibitor valproic acid (VPA) increased expression of BNIP3 in Raji cells at perinuclear locations. However antagonism between ATO and MG132 was increased in the presence of low doses of VPA. Addition of vincristine (VCR) blocked autophagy, while VPA+VCR treatment of Raji cells at sub-cytotoxic doses caused BNIP3 and mitochondria to redistribute to cytoplasmic peripheral location and increased mitochondrial mass. ATO+MG132 in the presence of subcytotoxic doses of VPA+VCR caused collapse of MMP in Raji cells, while interaction between ATO and MG132 shifted from antagonism to synergism. We conclude that synergism between ATO and MG132 was attained in Raji cells by disruption of the perinuclear mitochondrial cluster, blockage of selective autophagy of mitochondria (mitophagy) by VCR, increased mitochondrial mass, and upregulation of BNIP3 by VPA.
MeSH term(s)	Antineoplastic Combined Chemotherapy Protocols/pharmacology ; Arsenicals/pharmacology ; Autophagy/drug effects ; Cell Line, Tumor ; Cell Survival/drug effects ; Drug Synergism ; Enzyme Inhibitors/pharmacology ; Humans ; Leupeptins/pharmacology ; Membrane Potential, Mitochondrial/drug effects ; Membrane Potentials/drug effects ; Membrane Proteins/antagonists & inhibitors ; Membrane Proteins/metabolism ; Mitochondria/drug effects ; Oxides/pharmacology ; Proto-Oncogene Proteins/antagonists & inhibitors ; Proto-Oncogene Proteins/metabolism ; U937 Cells ; Up-Regulation ; Valproic Acid/administration & dosage ; Valproic Acid/pharmacology ; Vincristine/administration & dosage ; Vincristine/pharmacology
Chemical Substances	Arsenicals ; BNIP3 protein, human ; Enzyme Inhibitors ; Leupeptins ; Membrane Proteins ; Oxides ; Proto-Oncogene Proteins ; Vincristine (5J49Q6B70F) ; Valproic Acid (614OI1Z5WI) ; benzyloxycarbonylleucyl-leucyl-leucine aldehyde (RF1P63GW3K) ; arsenic trioxide (S7V92P67HO)
Language	English
Publishing date	2014-12
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	82061-1
ISSN	1879-0852 ; 0277-5379 ; 0959-8049 ; 0964-1947
ISSN (online)	1879-0852
ISSN	0277-5379 ; 0959-8049 ; 0964-1947
DOI	10.1016/j.ejca.2014.09.012
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Article ; Online: Haemostatic and immune role of cellular clotting in the sipunculan Themiste petricola.

Cavaliere, Victoria / Papademetrio, Daniela L / Alvarez, Elida M C / Blanco, Guillermo A

Cell and tissue research

2010 Volume 339, Issue 3, Page(s) 597–611

Abstract: Sipunculans, a small phylum of coelomated marine worms closely related to polychaete annelids, lack a true circulatory system. We have previously shown that the sipunculan Themiste petricola can form a cellular clot, without congealing, of cell-free ... ...

Abstract	Sipunculans, a small phylum of coelomated marine worms closely related to polychaete annelids, lack a true circulatory system. We have previously shown that the sipunculan Themiste petricola can form a cellular clot, without congealing, of cell-free coelomic fluid. The clot is formed by the aggregation of large granular leukocytes (LGLs) and may serve not only haemostatic but immune functions, since dissimilar particles may become entrapped within it. We have now evaluated the capacity of a massive clot, induced in vitro by sea water contact, to stop coelomic fluid flow. We have further studied smaller clots induced on glass-slides either with or without the presence of bacteria placed for entrapment within the clot. The fate of clotting LGLs is cell death while forming a cohesive mass, although cytoplasmic and nuclear remnants are shed from the clot. These remnants and any bacteria that avoid clot entrapment or are detached from the clot are engulfed by non-clotting cells that include small granular leukocytes (SGLs) and large hyaline amebocytes (LHAs). Both cell types can be found other than in the clot but SGLs also occur around the clot edges heavily loaded with engulfed material. The cytoskeletal arrangement of SGLs evaluated with phalloidin-rhodamine correspond to motile cells and contrast with that of clotting LGLs that form a massive network of F-actin. Thus, the complementary roles between clotting LGLs and non-clotting SGLs and LHAs act a central immune strategy of Themiste petricola to deal with body wall injury and pathogen intrusion into the coelomic cavity.
MeSH term(s)	Animals ; Bacteria/metabolism ; Blood Coagulation/immunology ; Cell Death ; Cell Line ; Cell Nucleus/metabolism ; Cytoskeleton/metabolism ; DNA Fragmentation ; Flow Cytometry ; Hemorheology ; Hemostasis/immunology ; Humans ; Leukocytes/cytology ; Leukocytes/microbiology ; Nematoda/cytology ; Nematoda/immunology ; Phagocytes ; Phagocytosis ; Seawater ; Yeasts/metabolism
Language	English
Publishing date	2010-03
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	125067-x
ISSN	1432-0878 ; 0302-766X
ISSN (online)	1432-0878
ISSN	0302-766X
DOI	10.1007/s00441-009-0912-9
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Article ; Online: Synergism between arsenite and proteasome inhibitor MG132 over cell death in myeloid leukaemic cells U937 and the induction of low levels of intracellular superoxide anion.

Lombardo, Tomás / Cavaliere, Victoria / Costantino, Susana N / Kornblihtt, Laura / Alvarez, Elida M / Blanco, Guillermo A

Toxicology and applied pharmacology

2012 Volume 258, Issue 3, Page(s) 351–366

Abstract: Increased oxygen species production has often been cited as a mechanism determining synergism on cell death and growth inhibition effects of arsenic-combined drugs. However the net effect of drug combination may not be easily anticipated solely from ... ...

Abstract	Increased oxygen species production has often been cited as a mechanism determining synergism on cell death and growth inhibition effects of arsenic-combined drugs. However the net effect of drug combination may not be easily anticipated solely from available knowledge of drug-induced death mechanisms. We evaluated the combined effect of sodium arsenite with the proteasome inhibitor MG132, and the anti-leukaemic agent CAPE, on growth-inhibition and cell death effect in acute myeloid leukaemic cells U937 and Burkitt's lymphoma-derived Raji cells, by the Chou-Talalay method. In addition we explored the association of cytotoxic effect of drugs with changes in intracellular superoxide anion (O₂⁻) levels. Our results showed that combined arsenite+MG132 produced low levels of O₂⁻ at 6h and 24h after exposure and were synergic on cell death induction in U937 cells over the whole dose range, although the combination was antagonistic on growth inhibition effect. Exposure to a constant non-cytotoxic dose of 80μM hydrogen peroxide together with arsenite+MG132 changed synergism on cell death to antagonism at all effect levels while increasing O₂⁻ levels. Arsenite+hydrogen peroxide also resulted in antagonism with increased O₂⁻ levels in U937 cells. In Raji cells, arsenite+MG132 also produced low levels of O₂⁻ at 6h and 24h but resulted in antagonism on cell death and growth inhibition. By contrast, the combination arsenite+CAPE showed high levels of O₂⁻ production at 6h and 24 h post exposure but resulted in antagonism over cell death and growth inhibition effects in U937 and Raji cells. We conclude that synergism between arsenite and MG132 in U937 cells is negatively associated to O₂⁻ levels at early time points after exposure.
MeSH term(s)	Antineoplastic Agents/administration & dosage ; Antineoplastic Agents/pharmacology ; Arsenites/pharmacology ; Burkitt Lymphoma/drug therapy ; Burkitt Lymphoma/pathology ; Cell Death/drug effects ; Cell Line, Tumor ; Dose-Response Relationship, Drug ; Drug Synergism ; Humans ; Hydrogen Peroxide/pharmacology ; Leukemia, Myeloid, Acute/drug therapy ; Leukemia, Myeloid, Acute/pathology ; Leupeptins/administration & dosage ; Leupeptins/pharmacology ; Reactive Oxygen Species/metabolism ; Sodium Compounds/pharmacology ; Superoxides/metabolism ; Time Factors ; U937 Cells
Chemical Substances	Antineoplastic Agents ; Arsenites ; Leupeptins ; Reactive Oxygen Species ; Sodium Compounds ; Superoxides (11062-77-4) ; sodium arsenite (48OVY2OC72) ; Hydrogen Peroxide (BBX060AN9V) ; benzyloxycarbonylleucyl-leucyl-leucine aldehyde (RF1P63GW3K)
Language	English
Publishing date	2012-02-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	204477-8
ISSN	1096-0333 ; 0041-008X
ISSN (online)	1096-0333
ISSN	0041-008X
DOI	10.1016/j.taap.2011.11.018
Database	MEDical Literature Analysis and Retrieval System OnLINE

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