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hepatoblastoma/глутатион
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Страница 1 от 45 полученные результаты
Acetaminophen-induced toxicity to human epidermoid cell line A431 and hepatoblastoma cell line Hep G2, in vitro, is diminished by silymarin.
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The skin and liver may be targets for cytotoxicity induced by oxidative drug metabolites. We used human epidermoid A431 cells and human hepatoblastoma Hep G2 cells as the experimental model. The aim of the study was to investigate and evaluate the effect of silymarin on acetaminophen (APAP)-induced
Identification of two activating elements in the proximal promoter region of the human glutathione transferase-A1 and -A2 genes.
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Promoter regions derived from the human glutathione S-transferase (GST) alpha gene cluster located on chromosome 6p12 were studied: the identical proximal promoters of the GST A1 and GST A2 genes and a proximal promoter of a pseudogene of this class. The sequence of the pseudogene promoter differs
Positive and negative regulatory regions in promoters of human glutathione transferase alpha genes.
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The human glutathione transferase (GST, EC 2.5.1.18) alpha class locus comprises several genes and pseudogenes. Genomic DNA encoding several human alpha-class-related genes and pseudogenes was cloned and characterized. Three distinct but highly similar 5'-flanking regions of GST alpha genes as well
Effect of selenium supplementation on the activities of glutathione metabolizing enzymes in human hepatoma Hep G2 cell line.
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Cell culture is an important tool for studying injury to cells exposed to oxidative stress. The human hepatoblastoma derived Hep G2 cells retain their morphology and most of their function in culture and are therefore widely used as an in vitro model of human hepatocytes. Conventional cell culture
Glutathione-S-transferase-pi expression regulates sensitivity to glutathione-doxorubicin conjugate.
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We have reported that glutathione-doxorubicin conjugate (GSH-DXR) exhibited potent cytotoxicity against tumor cells and inhibited glutathione-S-transferase (GST) enzyme activity. In order to determine whether or not the expression of GST-pi lowered the cytotoxicity of GSH-DXR, cytocidal activity of
Characterization of a class alpha glutathione-S-transferase with glutathione peroxidase activity in human liver microsomes.
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A 25.5kDa class alpha glutathione S-transferase (GST) designated as microsomal Ya-GST or M-GSTA has been purified to electrophoretic homogeneity from human liver microsomes. Limited proteolysis, gel filtration chromatography followed by EDTA, and alkaline Na(2)CO(3) treatments of microsomes indicate
Structure-activity relationships for the impact of selected isothiazol-3-one biocides on glutathione metabolism and glutathione reductase of the human liver cell line Hep G2.
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To investigate the toxic mode of action of isothiazol-3-one biocides the four compounds N-methylisothiazol-3-one (MIT), 5-chloro-N-methylisothiazol-3-one (CIT), N-octylisothiazol-3-one (OIT) and 4,5-dichloro-N-octylisothiazol-3-one (DCOIT) were purified and tested as single chemical entities for
Using acetaminophen's toxicity mechanism to enhance cisplatin efficacy in hepatocarcinoma and hepatoblastoma cell lines.
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OBJECTIVE
Acetaminophen overdose causes hepatotoxicity mediated by toxic metabolites generated through the cytochrome P450 enzyme. The objective of this study was to investigate whether acetaminophen (AAP) can enhance cisplatin (CDDP) cytotoxicity against human hepatocarcinoma and hepatoblastoma
Selenium supplementation attenuates procollagen-1 and interleukin-8 production in fat-loaded human C3A hepatoblastoma cells treated with TGFbeta1.
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BACKGROUND
Non-alcoholic fatty liver disease (NAFLD) is associated with obesity, insulin resistance and hepatic steatosis. Non-alcoholic steatohepatitis (NASH) is a serious consequence of NAFLD where chronic tissue damage and inflammation result in fibrosis which may progress to cirrhosis.
Role of Ca2+ influx in the tert-butyl hydroperoxide-induced apoptosis of HepG2 human hepatoblastoma cells.
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Oxidative stress appears to be implicated in the pathogenesis of various diseases including alcoholic liver injury. In this study we investigated the mechanism of apoptosis induced by tert-butyl hydroperoxide (TBHP) in HepG2 human hepatoblastoma cells. Treatment with TBHP significantly reduced
Copper resistant human hepatoblastoma mutant cell lines without metallothionein induction overexpress ATP7B.
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Mutant human hepatoblastoma cell lines resistant to copper toxicity were isolated from mutagenized HuH7. Two copper resistant cell lines (CuR), CuR 23 and CuR 27, had reduced basal expression of metallothionein (MT) messenger RNA (mRNA) and exhibited minimal or no increase in resistance to cadmium
Oxidative damage of mitochondrial and nuclear DNA induced by ionizing radiation in human hepatoblastoma cells.
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OBJECTIVE
Since reactive oxygen species (ROS) act as mediators of radiation-induced cellular damage, the aim of our studies was to determine the effects of ionizing radiation on the regulation of hepatocellular reduced glutathione (GSH), survival and integrity of nuclear and mitochondrial DNA
Chronic exposure of HepG2 cells to excess copper results in depletion of glutathione and induction of metallothionein.
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Metallothionein (MT) and reduced glutathione (GSH) play an important role in the intracellular handling of copper by preventing the generation and favouring the removal of copper-derived free radicals. The present study addressed the changes in MT and GSH that follow chronic (2 or 5 weeks) exposure
Nrf2 mediates the resistance of human A549 and HepG2 cancer cells to boningmycin, a new antitumor antibiotic, in vitro through regulation of glutathione levels.
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NF-E2-related factor 2 (Nrf2) is a transcription factor and a pivotal factor in the induction of the cell defense system. Recent reports show that Nrf2 plays critical roles in tumor heterogeneity and drug resistance. In the present study we investigated whether and how Nrf2 mediated the resistance
Altered expression of resistance associated genes in hepatoblastoma xenografts incorporated into mice following treatment with adriamycin or cisplatin.
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To study the development of drug resistance in childhood hepatoblastoma (HB) using a model closely related to in vivo conditions, we cultivated HB xenografts from 3 patients into mice and treated these tumors with either adriamycin (ADR) or cisplatin (CIS). Determination of the relative expression
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