oalib
Search Results: 1 - 10 of 100 matches for " "
All listed articles are free for downloading (OA Articles)
Page 1 /100
Display every page Item
PROTEN TYROSINE PHOSPHATASE ACTIVITY IN RAT ASCITES HEPATOMA CELLS
M.Saadat,D.D. Farhud
Iranian Journal of Public Health , 1998,
Abstract: Protein tyrosine phosphatases (PTPases) regulate tyrosine phosphorylation of target proteins involved in several aspects of cellular functions. Enzyme activities of the PTPases in cytosolic and particulate fractions of rat ascites hepatoma cell lines were determined and compared with those of normal rat liver. Our present data revealed that although there was no neoplatic-specific alteration of the PTPase activity in examined hepatomas, the activity in particulate fractions of island type of hepatomas was remarkably decreased compared with either rat liver or free type hepatomas.
Mechanism(s) of Toxic Action of Zn2+ and Selenite: A Study on AS-30D Hepatoma Cells and Isolated Mitochondria  [PDF]
Elena A. Belyaeva,Nils-Erik L. Saris
Biochemistry Research International , 2011, DOI: 10.1155/2011/387297
Abstract: Mitochondria of AS-30D rat ascites hepatoma cells are found to be the main target for Zn2
mRNA Levels of Related Abcb Genes Change Opposite to Each Other upon Histone Deacetylase Inhibition in Drug-Resistant Rat Hepatoma Cells  [PDF]
ádám Sike, Enik? Nagy, Balázs Vedelek, Dávid Pusztai, Péter Szerémy, Anikó Venetianer, Imre M. Boros
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0084915
Abstract: The multidrug-resistant phenotype of tumor cells is acquired via an increased capability of drug efflux by ABC transporters and causes serious problems in cancer treatment. With the aim to uncover whether changes induced by epigenetic mechanisms in the expression level of drug transporter genes correlates with changes in the drug resistance phenotypes of resistant cells, we studied the expression of drug transporters in rat hepatoma cell lines. We found that of the three major rat ABC transporter genes Abcb1a, Abcb1b and Abcc1 the activity of only Abcb1b increased significantly in colchicine-selected, drug-resistant cells. Increased transporter expression in drug-resistant cells results primarily from transcriptional activation. A change in histone modification at the regulatory regions of the chromosomally adjacent Abcb1a and Abcb1b genes differentially affects the levels of corresponding mRNAs. Transcriptional up- and down-regulation accompany an increase in acetylation levels of histone H3 lysine 9 at the promoter regions of Abcb1b and Abcb1a, respectively. Drug efflux activity, however, does not follow tightly the transcriptional activity of drug transporter genes in hepatoma cells. Our results point out the need for careful analysis of cause-and-effect relationships between changes in histone modification, drug transporter expression and drug resistance phenotypes.
Mechanism(s) of Toxic Action of Zn2+ and Selenite: A Study on AS-30D Hepatoma Cells and Isolated Mitochondria  [PDF]
Elena A. Belyaeva,Nils-Erik L. Saris
Biochemistry Research International , 2011, DOI: 10.1155/2011/387297
Abstract: Mitochondria of AS-30D rat ascites hepatoma cells are found to be the main target for Zn2+ and sodium selenite (Na2SeO3). High [mu]M concentrations of Zn2+ or selenite were strongly cytotoxic, killing the AS-30D cells by both apoptotic and necrotic ways. Both Zn2+ and selenite produced strong changes in intracellular generation of reactive oxygen species (ROS) and the mitochondrial dysfunction via the mitochondrial electron transport chain (mtETC) disturbance, the membrane potential dissipation, and the mitochondrial permeability transition pore opening. The significant distinctions in toxic action of Zn2+ and selenite on AS-30D cells were found. Selenite induced a much higher intracellular ROS level (the early event) compared to Zn2+ but a lower membrane potential loss and a lower decrease of the uncoupled respiration rate of the cells, whereas the mtETC disturbance was the early and critical event in the mechanism of Zn2+ cytotoxicity. Sequences of events manifested in the mitochondrial dysfunction produced by the metal/metalloid under test are compared with those obtained earlier for Cd2+, Hg2+, and Cu2+ on the same model system. 1. Introduction Zinc (Zn) and selenium (Se) are essential microelements with several important biological functions; among them are the maintenance of tissue integrity and function, proliferation, regulation of cellular thiol redox state, stabilization of intracellular environment, and protection against various stressors [1–4]. Despite Zn and Se are dietary nutrients for all mammalian species, an excess of these trace elements is harmful that produces the strong toxicity both to animals and humans and to the cultured cells. As well known now, the biological effects of Zn and Se are strictly dose dependent, with antioxidant properties at low concentrations and potent prooxidant effects at moderate to high concentrations. In particular, both Zn2+ and different Se compounds, especially sodium selenite (Na2SeO3), exhibit strong prooxidant effects on cells of different types that underlie, as generally accepted, for their anticancer activity [5–8]. However, the exact molecular mechanisms of toxic action of Zn2+ and selenite, namely, role of mitochondria and reactive oxygen species (ROS), the involvement of mitochondrial electron transport chain (mtETC), as well as sequences of events manifested in the mitochondrial dysfunction and cytotoxicity are not well understood up to date. So, using AS-30D rat ascites hepatoma cells cultivated in vitro, that is, the same model system as we applied in our previous works under studying the
Cirrhotic ascites
Sebati Ozdemir
Medical Journal of Bakirk?y , 2012,
Abstract: Ascites is the accumulation of free uid within the peritoneal cavity. In a patient with new-onset ascites, diagnostic paracentesis should be always performed regardless of the cause. Approximately 85% of cases of ascites are due to liver cirrhosis. In about 15% of patients with ascites, there is nonhepatic cause of uid retention. Ascites is the most common major complication of cirrhosis. Approximately 50% of patients with compensated cirrhosis develop ascites during 10 years of observation, and cirrhotic patients with ascites are associated with a 50% mortality over two years. In this article, clinic, pathophysiologic and diagnostic features and treatment of cirrhotic ascites are reviewed.
MANAGEMENT OF SYMPTOMATIC MALIGNANT ASCITES WITH DIURETICS AND PARACENTESIS: CASE REPORTS  [PDF]
Amer Hayat Khan,Andee Dzulkarnaen Zakaria,Syed Azhar Syed Sulaiman,Salleh S. Khairiyah
Journal of Pharmaceutical and Scientific Innovation , 2012,
Abstract: Malignant ascites is a widespread impediment of advanced cancer but to 20% of all cases of malignant ascites have unknown primary tumours. With the exception of ovarian cancer, the response of the ascites to treatment of the tumor is unsatisfactory and treatment related morbidity is common. The intent of most treatments for malignant ascites should be palliative with diuretics paracentesis were the common approach. A 53 years old, male patients who was admitted with history of abdominal distention for past 3 month associated with altered bowel habit and mucus per rectum and significant loss weight. Patients was diagnosed as malignant ascites with multicentric hepatoma with abdominal lymphodenopathy, lung, liver and vertebral body metastasis and left portal vein thrombosis. Patient was managed with temporary external paracentesis (pigtail catheter) and oral furosemide 40 mg daily and spironolactone 100 mg daily. Although abdominal paracentesis, diuretics and peritoneovenous shunting are commonly used procedures in management of malignant ascites, there are no randomized controlled trials evaluating the efficacy and safety of these therapies.
TUBERCULOUS ASCITES
ABDUL SATTAR
The Professional Medical Journal , 2004,
Abstract: Objectives: To assess the value of adenosine deaminase activity for the diagnosis oftuberculous ascites without performing peritoneal biopsy. Design: Prospective study. Setting: MedicalUnit IV Nishtar Hospital, Multan. Material and Methods: Fifty patients and fifty controls wereincluded in the study. The selection criteria for the patients were history, clinical examination andlymphocytic exudative ascites; and these were labeled as Group-A. While transudative ascites subjectswere kept as control and denoted as Group-B. ADA activity in the ascitic fluid of all the subjects ofGroup-A and Group-B was estimated by Giusti G method. The ADA activity of 40 u/L. Results werestatistically analyzed by applying chi square test. The results would be labeled statistically significant ifp value calculated was <0.05 Results: The ADA activity of the Group-A was 42.4±10.62 u/L while thatof Group-B was 20±10 u/L. Thirty-five in Group-A and five of Group-B had ADA activity above cutoff value (P <0.001). Conclusion: The results favour the application of ADA activity in ascitic fluid asthe diagnostic tool for tuberculosis ascites without performing an invasive procedure like peritonealbiopsy. The study revealed high levels of ADA activity in ascitic fluids of tuberculous patients ascompared to control group (having transudative ascites), 42.4±10.62 u/L and 20.0±10.0u/L respectively.
Ascites: Tips on diagnosis and management  [cached]
Al Mofleh Ibrahim,Al Rashed Rashed
Saudi Journal of Gastroenterology , 1996,
Abstract: Clinical evaluation and diagnostic paracentesis with estimation of the serum-ascitic albumin gradient (SAAG) is the most important step in identifying the etiology of ascites. At a level of 1.1 g/dl, SAAG, accurately (96.7%) differentiate portal hypertension from nonportal hypertension-associated ascites. The majority of patients with ascites (>80%) have portal hypertension associated etiology mainly, liver cirrhosis. Approximately 90% of patients with ascites complicating cirrhosis respond to salt restriction and diuretics. The remainder (10%),have refractory ascites which commonly respond well to large volume paracentesis (LVP). Asymptomatic complications occurring in patients treated with LVP may not necessitate treatment. Other alternative methods for treatment of refractory ascites include: ascitic fluid recirculation (AR), peritoneovenous shunting (PVS),transjugular intrahepatic portosystemic stent-shunting (TIPS) and orthotopic liver transplantation (OLT).
Effects of hypoxia-inducible factor-1α silencing on the proliferation of CBRH-7919 hepatoma cells  [cached]
Lin-Feng Xu,Jia-Yan Ni,Hong-Liang Sun,Yao-Ting Chen
World Journal of Gastroenterology , 2013, DOI: 10.3748/wjg.v19.i11.1749
Abstract: AIM: To study the effects of hypoxia-inducible factor-1α (HIF-1α) silencing on the proliferation of hypoxic CBRH-7919 rat hepatoma cells. METHODS: The CBRH-7919 rat hepatoma cell line was used in this study and the hypoxic model was constructed using CoCl2. The HIF-1α-specific RNAi sequences were designed according to the gene coding sequence of rat HIF-1α obtained from GeneBank. The secondary structure of the HIF-1α gene sequence was analyzed using RNA draw software. The small interfering RNA (siRNA) transfection mixture was produced by mixing the siRNA and Lipofectamine2000TM, and transfected into the hypoxic hepatoma cells. Real time reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting assay were used to detect the expression levels of mRNA and protein. HIF-1α and vascular endothelial growth factor (VEGF) mRNA was determined using real time RT-PCR; the protein expression levels of AKT, p-AKT, p21 and cyclinD1 were determined using Western blotting. The proliferation of hepatoma cells was observed using the methyl thiazolyl tetrazolium (MTT) assay and the bromodeoxyuridine (BrdU) incorporation cell proliferation assay. RESULTS: Under induced hypoxia, the viability of the hepatoma cells reached a minimum at 800 μmol/L CoCl2; the viability of the cells was relatively high at CoCl2 concentrations between 100 μmol/L and 200 μmol/L. Under hypoxia, the mRNA and protein expression levels of HIF-1α and VEGF were significantly higher than that of hepatoma cells that were cultured in normaxia. HIF-1α-specific RNAi sequences were successfully transfected into hepatoma cells. The transfection of specific siRNAs significantly inhibited the mRNA and protein expression levels of HIF-1α and VEGF, along with the protein expression levels of p-AKT and cyclinD1; the protein expression of p21 was significantly increased, and there was no significant difference in the expression of AKT. The MTT assay showed that the amount of hepatoma cells in S phase in the siRNA transfection group was obviously smaller than that in the control group; in the siRNA transfection group, the amount of hepatoma cells in G1 phase was more than that in the control group. The BrdU incorporation assay showed that the number of BrdU positive hepatoma cells in the siRNA transfection group was less than that in the control group. The data of the MTT assay and BrdU incorporation assay suggested that HIF-1α silencing using siRNAs significantly inhibited the proliferation of hepatoma cells. CONCLUSION: Hypoxia increases the expression of HIF-1α, and HIF-1α silencing significant
Glutathione Transferase (GST)-Activated Prodrugs  [PDF]
Paolo Ruzza,Andrea Calderan
Pharmaceutics , 2013, DOI: 10.3390/pharmaceutics5020220
Abstract: Glutathione transferase (formerly GST) catalyzes the inactivation of various electrophile-producing anticancer agents via conjugation to the tripeptide glutathione. Moreover, several data link the overexpression of some GSTs, in particular GSTP1-1, to both natural and acquired resistance to various structurally unrelated anticancer drugs. Tumor overexpression of these proteins has provided a rationale for the search of GST inhibitors and GST activated cytotoxic prodrugs. In the present review we discuss the current structural and pharmacological knowledge of GST-activated cytotoxic compounds.
Page 1 /100
Display every page Item


Home
Copyright © 2008-2017 Open Access Library. All rights reserved.