Results 171 to 180 of about 96,473 (194)
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Heme binding to Hep G2 human hepatoma cells
Journal of Hepatology, 1990Utilizing high specific activity [55Fe]hemin, the interaction of heme with monolayer cultures of human Hep G2 hepatoblastoma cells was examined. Initial characterization was performed at 4 degrees C to minimize the possibility of heme internalization. Specific binding of [55Fe]hemin at 4 degrees C reached equilibrium within 6 h and was 66% dissociable ...
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Antiproliferative effect of deferiprone on the Hep G2 cell line
Biochemical Pharmacology, 1998Iron is an essential element in cellular metabolism and the growth of all living species, and is involved in DNA replication. The risk of hepatocellular carcinoma development is associated with an increase in iron availability. The aim of the present work was to investigate the effect of an oral iron chelator, deferiprone (CP20), on HepG2 cell-line ...
N, Chenoufi +5 more
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Human phenolsulfotransferases: chiral substrates and expression in Hep G2 cells
Chemico-Biological Interactions, 1994Enzymatic sulfation of chiral phenolic ethanolamine drugs, e.g. beta-agonists, has been shown to be stereoselective in humans. The reaction appears to be specific for the monoamine (M) form of the phenol sulfotransferases (PSTs). In further studies of the stereochemistry of this reaction, we have found the hepatoblastoma-derived cell line Hep G2 to be ...
T, Walle +5 more
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Glycolate metabolism by Hep G2 cells.
Journal of the American Society of Nephrology : JASN, 1999The pathways of oxalate synthesis in humans are not well defined despite their clinical significance in primary hyperoxaluria and idiopathic calcium oxalate nephrolithiasis. Furthermore, the functional roles, if any, of this synthesis have not been elucidated.
R P, Holmes +4 more
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Mechanism of Impila (Callilepis laureola)-induced cytotoxicity in Hep G2 cells
Clinical Biochemistry, 2002To determine the mechanism(s) of Impila (Callilepis laureola)-induced toxicity in human hepatoblastoma Hep G2 cells in vitro and the possible prevention of this toxicity by N-acetylcysteine (NAC).Cells were treated with an aqueous extract of Impila (10 mg/mL) for up to 24 h.
Alpa, Popat +4 more
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Fatty acid uptake and metabolism in Hep G2 human-hepatoma cells
Molecular and Cellular Biochemistry, 1995The aim of this work was to study the fatty acid metabolism of the human-hepatoma cell line Hep G2. The cultured cells were incubated with either a saturated (palmitic, stearic) or a polyunsaturated (linoleic, alpha-linolenic, eicosatrienoic n-6) radioactive fatty acid.
C, Angeletti, M J, de Alaniz
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In vitro tumor necrosis factor cytotoxicity in HEP G2 liver cells
Hepatology, 1995Tumor necrosis factor-α(TNF-α) is a mediator of liver injury. The objective of this study was to develop an in vitro model of TNF-mediated liver cell injury using the Hep G2 cell line. Hep G2 cells normally are insensitive to TNF cytotoxicity, but they were rendered susceptible, or sensitized, to TNF cytotoxicity by inhibitors
D B, Hill +4 more
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Human hepatoma (Hep G2) cultures contain salt-resistant triglyceridase (“liver lipase”)
Life Sciences, 1986The culture fluid of Hep G2 human hepatoma cells contains triglyceridase activity resistant to high-salt concentrations. The lipase binds to Sepharose-heparin columns from which it can be eluted by 0.8 to 0.9 M NaCl. The nature of this lipase was studied using antibodies raised against "liver" lipases from human and rat origin.
N L, Persoon, H J, Sips, H, Jansen
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Tetrandrine-induced cell cycle arrest and apoptosis in Hep G2 cells
Life Sciences, 2003The effects of tetrandrine in the human hepatoblastoma G2 (Hep G2) cell line were investigated in this study. The results showed that tetrandrine not only inhibited Hep G2 growth but also induced apoptosis and blocked cell cycle progression in the G1 phase.
Po-Lin, Kuo, Chun-Ching, Lin
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Buckwheat trypsin inhibitor enters Hep G2 cells by clathrin-dependent endocytosis
Food Chemistry, 2013Recombinant buckwheat trypsin inhibitor (rBTI) was studied to evaluate if it could enter cancer cells and to determine the mechanism. Fluorescein isothiocyanate-labelled buckwheat trypsin inhibitor (FITC-BTI) entered Hep G2 cells in a concentration-dependent manner. FITC-BTI colocalised with labelled transferrin (Tf) in the punctate structure, implying
Xiaodong, Cui +3 more
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