Separate screening of brominated and chlorinated dioxins in field samples using in vitro reporter gene assays with rat and mouse hepatoma cell lines

2017 ◽  
Vol 975 ◽  
pp. 86-95
Author(s):  
Go Suzuki ◽  
Masafumi Nakamura ◽  
Chieko Michinaka ◽  
Nguyen Minh Tue ◽  
Hiroshi Handa ◽  
...  
Keyword(s):  
Cell Lines ◽  
Reporter Gene ◽  
Hepatoma Cell ◽  
Hepatoma Cell Lines ◽  
Mouse Hepatoma ◽  
Field Samples ◽  
Chlorinated Dioxins ◽  
Reporter Gene Assays

Looking for synergy or additivity between 188Re and sorafenib on hepatoma cell lines.

2012 ◽  
Vol 30 (4_suppl) ◽  
pp. 247-247
Author(s):  
Marc Pracht ◽  
Nicolas Lepareur ◽  
Julien Edeline ◽  
Laurence Lenoir ◽  
Valerie Ardisson ◽  
...  
Keyword(s):  
Cell Line ◽  
Hepg2 Cell ◽  
Cell Lines ◽  
Hepatoma Cell ◽  
External Beam Radiotherapy ◽  
Combined Treatment ◽  
Hepatoma Cell Lines ◽  
Heparg Cell Line

247 Background: In case of non resectable HCC, radioembolization and sorafenib (S) are therapeutic options respectively for intermediate and advanced stages. In some other cancers, there is an increase of efficacy when external beam radiotherapy is done concomitantly with systemic chemotherapy or targeted therapies. So we wondered if there could be a synergistic or an additive activity when S is combined with a radionuclide. Methods: Hepatoma cell lines N1S1 (murine HCC), HepG2 (human hepatoblastoma) and HepaRG (human HCC) were treated with increasing concentrations of rhenium-188 (188Re) or S. On each cell line, we have studied the cellular toxicities of S and 188Re using Tetrazolium dye test, extra-cellular medium LDH level and morphologic analysis. This was done for different dosage of S and 188Re. We measured the lethal concentration killing 25% of cells (LC25) with the results of the Tetrazolium dye test. Secondly, we looked for synergy or additivity on cellular toxicity of these two compounds according to cell lines by combined treatment. Synergy or additivity was estimated with the combination index (CI) method (synergy if CI lower than 1, additivity if CI = 1, antagonism if CI upper to 1) based on the Tetrazolium dye test’s results. Results: Monotherapy dose-dependent toxicities were observed for all three cell lines with 188Re and for the N1S1 and HepG2 cell lines only with S. Combined treatment with 188Re and S showed synergy on HepaRG and N1S1 cell lines and additivity on the HepG2 cell line. Conclusions: The additive, and even synergistic, interest of a combined treatment with 188Re and S is demonstrated in vitro (for the first time to our knowledge) on hepatoma cell lines. This results, in particular for the HepaRG cell line (human HCC), could be explained by the down-regulation of the hepatic drug transporters which are responsible for the Sorafenib efflux in case of simultaneous DNA damages due to a radionuclide exposition. This promising approach now needs to be confirmed in vivo. [Table: see text]

The CALUX bio-assay: Analytical comparison between mouse hepatoma cell lines with a low (H1L6.1c3) and high (H1L7.5c1) number of dioxin response elements

Talanta ◽  
2011 ◽  
Vol 85 (4) ◽  
pp. 2039-2046 ◽  
Author(s):  
Kersten Van Langenhove ◽  
Kim Croes ◽  
Michael S. Denison ◽  
Marc Elskens ◽  
Willy Baeyens
Keyword(s):  
Cell Lines ◽  
Hepatoma Cell ◽  
Response Elements ◽  
Analytical Comparison ◽  
Hepatoma Cell Lines ◽  
Mouse Hepatoma ◽  
Bio Assay

scholarly journals AS-30D hepatoma as a model to study on insulin resistance in vitro.

2013 ◽  
Vol 60 (4) ◽  
Author(s):  
Katarzyna Wierzbicka-Bregier ◽  
Wojciech Brutkowski ◽  
Anna Borkowska ◽  
Krzysztof Milewski ◽  
Krzysztof Zabłocki
Keyword(s):  
Insulin Resistance ◽  
Cell Lines ◽  
Hepatoma Cell ◽  
Cellular Level ◽  
Ros Generation ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Hepatoma Cell Lines ◽  
Kinase Phosphorylation

Studies on insulin resistance of liver cells are often performed with the use of various hepatoma cell lines. Such an approach allows investigating selected biochemical pathways at the cellular level. However, possible modifications of metabolic processes due to the neoplastic nature of such cells must be considered. Expanding the diversity of hepatoma cell lines used in metabolic studies could deliver new data for comparison with those obtained for other cell lines and should reduce the risk of misleading conclusions. In this study rat hepatoma AS-30D cells were tested as a potential model for studies on palmitate-induced insulin resistance. It was found that insulin-induced Akt kinase phosphorylation was substantially reduced in cells incubated with palmitate at a concentration as low as 75 µM. This effect was not accompanied by excessive reactive oxygen species (ROS) generation or increased Jun N-terminal kinase (JNK) phosphorylation. Moreover, preincubation of AS-30D cells with rosiglitazone, an antidiabetic agonist of peroxisome proliferator-activated receptor gamma (PPARγ), efficiently prevented the palmitate-induced insulin resistance. We conclude that AS-30D hepatoma cells may be used as a model sensitive to insulin and vulnerable to palmitate-induced insulin resistance.

Non-genotoxic hepatocarcinogenesis in vitro: the FaO hepatoma line responds to peroxisome proliferators and retains the ability to undergo apoptosis

1993 ◽  
Vol 104 (2) ◽  
pp. 307-315 ◽  
Author(s):  
A.C. Bayly ◽  
N.J. French ◽  
C. Dive ◽  
R.A. Roberts
Keyword(s):  
Cell Death ◽  
Cell Line ◽  
Cell Lines ◽  
Hepatoma Cell ◽  
Hepatoma Cell Line ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferators ◽  
Hepatoma Cell Lines

A range of hepatoma cell lines (RH1, HTC, FaO, 7800C1 and MH1C1), has been studied with the aim of establishing an in vitro model to investigate the molecular mechanisms of hepatocarcinogenicity induced by the peroxisome proliferator class of non-genotoxic carcinogens. In view of speculation that peroxisome proliferators suppress hepatocyte apoptosis in vivo, we have placed particular emphasis on evaluating whether hepatoma cell lines retain the ability to undergo apoptotic cell death. Expression of the liver-specific differentiation marker albumin and the peroxisome proliferator-activated receptor (PPAR) was highest in the Reuber hepatoma cell line, FaO. This cell line also demonstrated the most marked response to the peroxisome proliferator nafenopin with a 2.2-fold induction of the microsomal enzyme cytochrome p450IVA1. This response was found to display intercellular heterogeneity by immunocytochemistry. Thus, the FaO cell line maintained characteristics of hepatocytes, both in vivo and in vitro, in terms of expression of constitutive and inducible markers. However, none of the cell lines tested mirrored the hyperplastic response of hepatocytes to nafenopin, since no increase in cell growth kinetics was observed on addition of nafenopin to the growth medium. The mode of cell death in confluent FaO cultures was characterised as apoptosis, by fluorescence microscopy and agarose gel electrophoresis of extracted DNA. Cells detaching from confluent FaO cultures exhibited chromatin condensation and DNA fragmentation patterns characteristic of cels undergoing apoptotic death.Interestingly, no apoptosis was seen in monolayer cells, suggesting that apoptosis in vitro is associated with cell shrinkage and detachment similar to that documented for the liver in vivo.(ABSTRACT TRUNCATED AT 250 WORDS)

Human hepatoma cell lines on gas foaming templated alginate scaffolds for in vitro drug-drug interaction and metabolism studies

2015 ◽  
Vol 30 (1) ◽  
pp. 331-340 ◽  
Author(s):  
A. Stampella ◽  
G. Rizzitelli ◽  
F. Donati ◽  
M. Mazzarino ◽  
X. de la Torre ◽  
...  
Keyword(s):  
Drug Interaction ◽  
Cell Lines ◽  
Hepatoma Cell ◽  
Human Hepatoma ◽  
Human Hepatoma Cell ◽  
Hepatoma Cell Lines ◽  
Drug Drug Interaction ◽  
Gas Foaming
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