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1
المؤلفون: Elisabetta Carata, Elisa Panzarini, Viviana Vergaro, Francesco Mura, Gian Maria Fimia, Luciana Dini, Marco Corazzari, Giuseppe Ciccarella, Stefania Mariano, Cristian Vergallo, Marco Rossi
المساهمون: Panzarini, Elisa, Mariano, Stefania, Vergallo, Cristian, Carata, Elisabetta, Fimia, Gian Maria, Mura, F, Rossi, M, Vergaro, Viviana, Ciccarella, Giuseppe, Corazzari, M, Dini, Luciana
المصدر: Toxicology in Vitro. 41:64-74
مصطلحات موضوعية: 0301 basic medicine, Silver, Cell cycle checkpoint, Cell Survival, Population, Cell, Metal Nanoparticles, Antineoplastic Agents, 02 engineering and technology, Toxicology, Silver nanoparticle, HeLa, 03 medical and health sciences, Microscopy, Electron, Transmission, medicine, Humans, Viability assay, education, Cytotoxicity, Cell cycleCytotoxicityHeLa cellsNanoparticles uptakeSilver nanoparticles (AgNPs), education.field_of_study, L-Lactate Dehydrogenase, biology, Chemistry, Cell Cycle Checkpoints, General Medicine, Cell cycle, 021001 nanoscience & nanotechnology, biology.organism_classification, Glucose, 030104 developmental biology, medicine.anatomical_structure, Biochemistry, Biophysics, 0210 nano-technology, HeLa Cells
الوصف: This study aims to determine the interaction (uptake and biological effects on cell viability and cell cycle progression) of glucose capped silver nanoparticles (AgNPs-G) on human epithelioid cervix carcinoma (HeLa) cells, in relation to amount, 2 × 10 3 or 2 × 10 4 NPs/cell, and exposure time, up to 48 h. The spherical and well dispersed AgNPs (30 ± 5 nm) were obtained by using glucose as reducing agent in a green synthesis method that ensures to stabilize AgNPs avoiding cytotoxic soluble silver ions Ag + release. HeLa cells take up abundantly and rapidly AgNPs-G resulting toxic to cells in amount and incubation time dependent manner. HeLa cells were arrested at S and G2/M phases of the cell cycle and subG1 population increased when incubated with 2 × 10 4 AgNPs-G/cell. Mitotic index decreased accordingly. The dissolution experiments demonstrated that the observed effects were due only to AgNPs-G since glucose capping prevents Ag + release. The AgNPs-G influence on HeLa cells viability and cell cycle progression suggest that AgNPs-G, alone or in combination with chemotherapeutics, may be exploited for the development of novel antiproliferative treatment in cancer therapy. However, the possible influence of the cell cycle on cellular uptake of AgNPs-G and the mechanism of AgNPs entry in cells need further investigation.
وصف الملف: ELETTRONICO
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::5651b166c168b675d1644baf80f58264Test
https://doi.org/10.1016/j.tiv.2017.02.014Test -
2
المؤلفون: Angelika Bondzio, Ralf Einspanier, F. Scharfen, Ulrike Lodemann, Holger Martens
المصدر: Toxicology in Vitro. 27:834-843
مصطلحات موضوعية: Cell Survival, Swine, Cell Culture Techniques, chemistry.chemical_element, Zinc, Biology, Toxicology, medicine.disease_cause, Cell Line, chemistry.chemical_compound, Adenosine Triphosphate, Lactate dehydrogenase, medicine, Animals, Humans, HSP70 Heat-Shock Proteins, RNA, Messenger, Viability assay, Barrier function, Cell Proliferation, L-Lactate Dehydrogenase, Epithelial Cells, General Medicine, In vitro, Cell biology, Intestines, chemistry, Biochemistry, Caco-2, Cell culture, Zinc toxicity, Caco-2 Cells
الوصف: Zinc is an essential trace element with a variety of physiological and biochemical functions. Piglets are commonly supplemented, during the weaning period, with doses of zinc above dietary requirements with positive effects on health and performance that might be attributed to anti-secretory and barrier-enhancing effects in the intestine. For a better understanding of these observations increasing zinc sulfate (ZnSO4; 0-200μM) concentrations were used in an in vitro culture model of porcine (IPEC-J2) and human (Caco-2) intestinal epithelial cells and effects on barrier function, viability, and the mRNA expression of one selected heat shock protein (Hsp) were assessed. When treated apically with zinc sulfate, the transepithelial electrical resistance (TEER) did not change significantly. In contrast, cell viability measured by lactate dehydrogenase (LDH) leakage, by ATP and by WST-1 conversion in postconfluent IPEC-J2 monolayers was affected after a 24-h treatment with 200μM ZnSO4. Caco-2 cells were more resistant to Zn. ZnSO4 did not induce any effect on viability, except when it was used at the highest concentration (200μM), and only in preconfluent cells. Furthermore, ZnSO4 induced Hsp70 mRNA expression at 200μM and was more pronounced in preconfluent cells. The observed dose-related effects of zinc are cell-line specific and depended on the differentiation status of the cells. The IPEC-J2 cell line appears to be a suitable in vitro model to characterize specific effects on porcine intestinal cells.
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::37150d98e32f29e6e8f47f82f1d2ddccTest
https://doi.org/10.1016/j.tiv.2012.12.019Test -
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المؤلفون: László G. Puskás, Levente Kürti, Szilvia Veszelka, Ngo Thi Khue Dung, Ágnes Kittel, Piroska Szabó-Révész, Mária A. Deli, Alexandra Bocsik, Béla Ózsvári
المصدر: Toxicology in Vitro. 26:445-454
مصطلحات موضوعية: Sucrose, Polysorbates, Excipient, Toxicology, Permeability, Cell Line, Polyethylene Glycols, Excipients, chemistry.chemical_compound, Drug Delivery Systems, Pulmonary surfactant, Lactate dehydrogenase, medicine, Humans, Chromatography, Dose-Response Relationship, Drug, L-Lactate Dehydrogenase, Dextrans, General Medicine, Nasal Mucosa, Dextran, chemistry, Biochemistry, Permeability (electromagnetism), Paracellular transport, Drug delivery, Fluorescein-5-isothiocyanate, medicine.drug
الوصف: Sucrose esters are effective solubilizers and there is an interest to use them as pharmaceutical excipients for nasal drug delivery. We have determined for the first time the non-toxic doses of laurate and myristate sucrose esters by four independent methods, and their effects on epithelial permeability using RPMI 2650 human nasal epithelial cell line. Based on real-time cell electronic sensing, MTT dye conversion and lactate dehydrogenase release methods reference surfactant Cremophor RH40 proved to be the least toxic excipient, and could be used at 5mg/mL concentration for 1h in epithelial cells without cellular damage. The non-toxic dose of Tween 80 was 1 mg/mL, while the dose of laurate and myristate sucrose esters that could be safely used on cells for 1 h was 0.1 mg/mL. Both the reference surfactants and the sucrose esters significantly enhanced the permeability of epithelial cell layers for the paracellular marker FITC-labelled 4.4 kDa dextran at 0.1 mg/mL concentration. The effects of sucrose esters on epithelial permeability were dose-dependent. These data indicate that laurate and myristate sucrose esters can be potentially used as permeability enhancers in nasal formulations to augment drug delivery to the systemic circulation.
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::fe0b99dd63729be0cef8a14549f80db6Test
https://doi.org/10.1016/j.tiv.2012.01.015Test -
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المصدر: Toxicology in Vitro. 25:1061-1066
مصطلحات موضوعية: Male, Antifungal Agents, Necrosis, Neutrophils, Rutin, Caspase 3, Pharmacology, Toxicology, Cell Line, Nephrotoxicity, chemistry.chemical_compound, Thiabendazole, Lactate dehydrogenase, medicine, Animals, Viability assay, Rats, Wistar, Biotransformation, Peroxidase, Caspase 7, L-Lactate Dehydrogenase, biology, Epithelial Cells, General Medicine, Rats, Biochemistry, chemistry, Apoptosis, Myeloperoxidase, Toxicity, biology.protein, medicine.symptom
الوصف: Thiabendazole (TBZ), an antihelminthic and antifungal agent, is associated with a host of adverse effects including nephrotoxicity, hepatotoxicity, and teratogenicity. Bioactivation of the primary metabolite of TBZ, 5-hydroxythiabendazole, has been proposed to yield a reactive intermediate. Here we show that this reactive intermediate can be catalyzed by myeloperoxidase (MPO), a neutrophil-bourne peroxidase. Using a cell viability endpoint, we examined the toxicity of TBZ, 5OH-TBZ, and MPO-generated metabolites in cell-based models including primary rat proximal tubule epithelial cells, NRK-52E rat proximal tubule cells, and H9C2 rat myocardial cells. Timecourse experiments with MPO showed complete turnover of 5OH-TBZ within 15 min and a dramatic leftward shift in dose–response curves after 12 h. After a 24 h exposure in vitro , the LC 50 of this reactive intermediate was 23.3 ± 0.2 μM reduced from greater than 200 μM from 5OH-TBZ alone, an approximately 10-fold decrease. LC 50 values were equal in all cell types used. Comparison of lactate dehydrogenase leakage and caspase 3/7 activity revealed that cell death caused by the reactive intermediate is primarily associated with necrosis rather than apoptosis. This toxicity can be completely rescued via incubation with rutin, an inhibitor of MPO. These results suggest that MPO-mediated biotransformation of 5OH-TBZ yields a reactive intermediate which may play a role in TBZ-induced toxicity.
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::93bd4d3e51dcfbf70bbf760b98ef6e08Test
https://doi.org/10.1016/j.tiv.2011.04.007Test -
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المؤلفون: Maqusood Ahamed
المصدر: Toxicology in Vitro. 25:930-936
مصطلحات موضوعية: Time Factors, Metal Nanoparticles, Toxicology, medicine.disease_cause, chemistry.chemical_compound, Nickel, Lactate dehydrogenase, medicine, Humans, MTT assay, Cytotoxicity, Lung, chemistry.chemical_classification, A549 cell, Inhalation Exposure, Reactive oxygen species, Dose-Response Relationship, Drug, L-Lactate Dehydrogenase, technology, industry, and agriculture, Epithelial Cells, General Medicine, Glutathione, respiratory system, Molecular biology, Mitochondria, Oxidative Stress, chemistry, Biochemistry, Toxicity, Lipid Peroxidation, Reactive Oxygen Species, Oxidative stress
الوصف: Nickel nanoparticle (Ni NP) is increasingly used in modern industries such as catalysts, sensors and electronic applications. Due to wide-spread industrial applications the inhalation is the primary source of exposure to Ni NPs. However, data demonstrating the effect of Ni NPs on the pulmonary system remain scarce. The present study was designed to examine the toxic effect of human lung epithelial A549 cells treated with well characterized Ni NPs at the concentrations of 0, 1, 2, 5, 10 and 25 μg/ml for 24 and 48 h. Mitochondrial function (MTT assay), membrane leakage of lactate dehydrogenase (LDH assay), reduced glutathione (GSH), reactive oxygen species (ROS), membrane lipid peroxidation (LPO) and caspase-3 activity were assessed as toxicity end points. Results showed that Ni NPs reduced mitochondrial function and induced the leakage of LDH in dose and time-dependent manner. Ni NPs were also found to induce oxidative stress in dose and time-dependent manner indicated by depletion of GSH and induction of ROS and LPO. Further, activity of caspase-3 enzyme, marker of apoptosis was significantly higher in treated cells with time and Ni NPs dosage. The results exhibited significant toxicity of Ni NPs in human lung epithelial A549 cells which is likely to be mediated through oxidative stress. This study warrants more careful assessment of Ni NPs before their industrial applications.
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::c1f9a3a9a9fca1e571edd3ce36329435Test
https://doi.org/10.1016/j.tiv.2011.02.015Test -
6
المؤلفون: Xiaolian Shi, Jiye Zhang, Mao Youhua, Qiao-Li Ji, Rong Lin, Xiaogang Zhai, Qinqin Lin
المصدر: Toxicology in Vitro. 24:1086-1091
مصطلحات موضوعية: Cell Survival, Gene Expression, Pharmacology, Toxicology, chemistry.chemical_compound, Carnitine palmitoyltransferase 1, Lactate dehydrogenase, Toxicity Tests, Cytochrome P-450 CYP1A1, medicine, Humans, Aspartate Aminotransferases, Viability assay, ATP Binding Cassette Transporter, Subfamily G, Member 1, Valproic Acid, Carnitine O-Palmitoyltransferase, L-Lactate Dehydrogenase, biology, Fatty acid metabolism, Fatty Acids, Cytochrome P450, Alanine Transaminase, Transporter, Hep G2 Cells, General Medicine, Lipid Metabolism, digestive system diseases, Liver, Biochemistry, ABCG1, chemistry, biology.protein, ATP-Binding Cassette Transporters, Anticonvulsants, lipids (amino acids, peptides, and proteins), medicine.drug
الوصف: The hepatotoxicity induced by valproic acid (VPA) has been described in many clinical studies and the related mechanism has been partly elucidated. The objective of this study is to investigate the hepatotoxicity and its underlying mechanism of valproic acid on human hepatoma carcinoma cell line HepG2. The cell viability was evaluated by 3-(4,5-dimethyltyiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) in the medium were detected using spectrophotometry. The gene expressions of cytochrome P450 1 A1 (CYP1A1), ATP-binding cassette transporter G1 (ABCG1) and carnitine palmitoyltransferase 1 (CPT1A), related to lipid transport and fatty acid metabolism, were measured by quantitative real-time reverse transcriptase-PCR. Treatment with valproate sodium obviously decreased the viability of HepG2 cells, accompanied by the increased leakages of ALT, AST and LDH in a dose-dependent manner. Furthermore, the gene expressions of CYP1A1, ABCG1 and CPT1A were almost up-regulated in the treated groups. In conclusion, these data suggest that VPA-induced hepatotoxicity was critically enhanced with the elevation of valproate sodium, which may be correlated with up-regulated gene expressions of CYP1A1, ABCG1 and CPT1A.
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::8aaec2675195c2d822ce0dbe54a0955cTest
https://doi.org/10.1016/j.tiv.2010.03.014Test -
7
المؤلفون: Jean-Luc Brunet, Alexandra Badiou, Cyril Vidau, Luc P. Belzunces
المساهمون: Abeilles et Environnement (AE), Institut National de la Recherche Agronomique (INRA)-Avignon Université (AU)
المصدر: Toxicology in Vitro
Toxicology in Vitro, Elsevier, 2009, 23, pp.589-597. ⟨10.1016/j.tiv.2009.01.017⟩مصطلحات موضوعية: Insecticides, CACO-2 CELL, LDH, [SDV]Life Sciences [q-bio], FIPRONIL, ENERGETIC METABILISM, Biology, Toxicology, INTESTINAL EPITHELIUM, EPITHELIUM INTESTINAL, chemistry.chemical_compound, Adenosine Triphosphate, SULFONE, SULFIDE, Electric Impedance, Humans, CYTOTOXICITY, Lactic Acid, Viability assay, PHENYLPYRAZOLE, Cytotoxicity, TEER, Barrier function, Fipronil, Cell Proliferation, Dose-Response Relationship, Drug, L-Lactate Dehydrogenase, TRANSEPITHELIAL ELECTRIC RESISTANCE, LACTATE DEHYDROGENASE, HUMAN, Epithelial Cells, CELLULE CACO-2, General Medicine, Metabolism, ETHIPROL, Intestinal epithelium, Mitochondria, ATP, METABOLITE, INTESTIN, Biochemistry, chemistry, INSECTICIDE, Caco-2, CYTOTOXICITE, Pyrazoles, Caco-2 Cells, Energy Metabolism, Xenobiotic
الوصف: Phenylpyrazoles are relatively new insecticides designed to manage problematic insect resistance and public health hazards encountered with older pesticide families. In vitro cytotoxicity induced by the phenylpyrazole insecticides, Ethiprol and Fipronil, and Fipronil metabolites, sulfone and sulfide, was studied in Caco-2 cells. This cellular model was chosen because it made possible to mimic the primary site of oral exposure to xenobiotics, the intestinal epithelium. Assessment of the barrier function of Caco-2 epithelium was assessed by TEER measurement and showed a major loss of barrier integrity after exposure to Fipronil and its metabolites, but not to Ethiprol. The disruption of the epithelial barrier was attributed to severe ATP depletion independent of cell viability, as revealed by LDH release. The origin of energetic metabolism failure was investigated and revealed a transient enhancement of tetrazolium salt reduction and an increase in lactate production by Caco-2 cells, suggesting an increase in glucose metabolism by pesticides. Cellular symptoms observed in these experiments lead us to hypothesize that phenylpyrazole insecticides interacted with mitochondria
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::445b589cb2fd8177907a105cc5c96666Test
https://doi.org/10.1016/j.tiv.2009.01.017Test -
8
المصدر: Toxicology in Vitro. 18:285-292
مصطلحات موضوعية: Kidney Cortex, Time Factors, Cell Survival, Glutamine, In Vitro Techniques, Biology, Toxicology, Cryopreservation, Andrology, chemistry.chemical_compound, Adenosine Triphosphate, Lactate dehydrogenase, Humans, Carbon Radioisotopes, Alanine, L-Lactate Dehydrogenase, Valproic Acid, Glutamate dehydrogenase, Glutamate receptor, Proteins, General Medicine, Gluconeogenesis, chemistry, Biochemistry, Intracellular
الوصف: We have tested the suitability of cryopreserved human precision-cut renal cortical slices for metabolic and pharmaco-toxicological studies. The viability of these slices and their pharmaco-toxicological reactivity were assessed using intracellular ATP and protein contents, lactate dehydrogenase (LDH) leakage, lactate and glutamine metabolism and the ammoniagenic effect of valproate. Despite a decrease in ATP and protein contents when compared with those of fresh slices, cryopreserved slices did not show any LDH leakage and retained the capacity to metabolize glutamine and lactate. Glutamine removal and ammonia, lactate and alanine production were similar in fresh and cryopreserved slices; by contrast, cryopreserved slices accumulated more glutamate as a result of decreased flux through glutamate dehydrogenase which catalyses an oxygen-dependent reaction. Valproate markedly and similarly stimulated glutamine metabolism in fresh and cryopreserved slices. Cryopreservation did not alter lactate removal but inhibited lactate gluconeogenesis. In conclusion, these results demonstrate that, although their mitochondrial oxidative metabolism seems to be diminished, cryopreserved human precision-cut renal cortical slices remain metabolically viable and retain the capacity to respond to the ammoniagenic effect of valproate. Thus, this experimental model may be helpful to optimize the use of human renal tissue for metabolic and pharmaco-toxicological studies.
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::70d3df886f41a949fb5187d716c7b719Test
https://doi.org/10.1016/j.tiv.2003.08.010Test -
9
المؤلفون: Daniel Junqueira Dorta, Lilian Cristina Pereira, Alecsandra Oliveira de Souza, Danielle Palma de Oliveira
المصدر: Repositório Institucional da USP (Biblioteca Digital da Produção Intelectual)
Universidade de São Paulo (USP)
instacron:USPمصطلحات موضوعية: Cell death, Programmed cell death, Apoptosis, APOPTOSE, Toxicology, chemistry.chemical_compound, Polybrominated diphenyl ethers, Halogenated Diphenyl Ethers, Humans, HepG2 cells, Caspase, Cell Proliferation, Flame Retardants, Cell Nucleus, Membrane Potential, Mitochondrial, biology, L-Lactate Dehydrogenase, Cell growth, Caspase 3, BDE-99, Cell Membrane, ROS, General Medicine, Phosphatidylserine, Hep G2 Cells, Caspase 9, Biochemistry, chemistry, Toxicity, biology.protein, DNA fragmentation, Reactive Oxygen Species
الوصف: Polybrominated Diphenyl Ethers (PBDEs) are an important class of flame retardants with a wide range of toxic effects on biotic and abiotic systems. The toxic mechanisms of PBDEs are still not completely understood because there are several different congeners with different chemical and biological characteristics. BDE-99 is one of these, widely found in the environment and biological samples, showing evidence of neurotoxic and endocrine disruption activities, but with little information about its action mechanism described in the current literature. This work investigated the effects of BDE-99 on the HepG2 cell line in order to clarify its toxic mechanism, using concentrations of 0.5–25μM (24 and 48h). Our results showed that BDE-99 could cause cell death in the higher concentrations, its activity being related to a decrease in mitochondrial membrane potential and an accumulation of ROS. It was also shown that BDE-99 induced the exposure of phosphatidylserine, caspases 3 and 9 activation and DNA fragmentation in HepG2 cells, without causing the release of LDH. Thus it was shown that BDE-99 could cause HepG2 cell death by apoptosis, suggesting its toxicity to the human liver.
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::689c644760c20ff9a02c676d182d3b8bTest
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10
المؤلفون: R. Bars, C. Dilworth, D. Bigot-Lasserre
المصدر: Toxicology in Vitro. 15:623-630
مصطلحات موضوعية: Male, Programmed cell death, Necrosis, Apoptosis, Nitric Oxide, Toxicology, Nitric oxide, Transforming Growth Factor beta1, chemistry.chemical_compound, Adenosine Triphosphate, Glycochenodeoxycholic Acid, Transforming Growth Factor beta, Lactate dehydrogenase, medicine, Animals, Rats, Wistar, Nitrite, Cells, Cultured, L-Lactate Dehydrogenase, biology, Caspase 3, General Medicine, Glutathione, Molecular biology, Rats, Nitric oxide synthase, NG-Nitroarginine Methyl Ester, medicine.anatomical_structure, Biochemistry, chemistry, Caspases, Hepatocyte, Hepatocytes, biology.protein, medicine.symptom
الوصف: Primary cultures of hepatocytes are a widely used in vitro model for biochemical research. Following isolation, hepatocytes produce large amounts of nitric oxide (NO), which is known to have both pro- and anti-apoptotic effects in hepatocytes in vivo and in vitro. Previous work has not determined the effect of these increased levels of NO on the response of hepatocytes to apoptotic stimuli. Here we report that levels of nitrites are elevated in hepatocyte monolayers from 24 h onwards. Addition of the inducible nitric oxide synthase (iNOS) inhibitor, Nomega-nitro-L-arginine methyl ester (L-NAME), to the medium inhibited this increase in nitrites. These results indicate that the increase in nitrite is most likely due to the formation of NO. Elevated nitrite levels had no effect either on basal levels of apoptosis or on ATP and GSH. Apoptosis was induced by transforming growth factor beta-1 (TGFbeta-1) or glycochenodeoxycholate (GCDC). Both compounds caused moderate hepatocyte apoptosis; however, addition of L-NAME prior to exposure significantly increased the level of apoptosis observed with the two compounds. Both TGFbeta-1 and GCDC had no effect on hepatocyte ATP or GSH levels; however, as a consequence of secondary necrosis, TGFbeta-1 exposure significantly increased levels of lactate dehydrogenase (LDH) leakage. These findings indicate that the increased levels of NO associated with the culture of hepatocytes have an inhibitory effect on compound-induced apoptosis in the cells.
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::09c7cf35bd2f37b78b1f22951a0169d1Test
https://doi.org/10.1016/s0887-2333Test(01)00088-1
